17:I[462708,["/_next/static/chunks/3yo3kiro3bmlp.js","/_next/static/chunks/3vr2wvd8f2efb.js","/_next/static/chunks/2vtmb68_vu-9t.js","/_next/static/chunks/2s8mt6_8wrpfo.js","/_next/static/chunks/3vkulz2i3l61y.js","/_next/static/chunks/1cqw2i1silz0i.js","/_next/static/chunks/14dbm3lm_t629.js","/_next/static/chunks/335_v2mb569ld.js","/_next/static/chunks/3ykn5ops9bft5.js","/_next/static/chunks/3cmavum774kjt.js","/_next/static/chunks/3th-0-a2xf9qs.js","/_next/static/chunks/0p0xpwde6kzmv.js","/_next/static/chunks/401-sxxnzbtf_.js","/_next/static/chunks/0wywtv698a1v0.js","/_next/static/chunks/2botzqwpnrzyj.js"],"ArticleReader"] 18:T62ff,## Summary Type 2 diabetes mellitus (T2D) is chronic hyperglycemia caused by progressive beta-cell dysfunction on a background of insulin resistance and broader metabolic dysregulation. Diagnosis in a nonpregnant person is established by **A1C ≥6.5% (48 mmol/mol)**, **fasting plasma glucose ≥126 mg/dL (7.0 mmol/L)**, **2-hour plasma glucose ≥200 mg/dL (11.1 mmol/L) during a 75-g oral glucose tolerance test**, or **random plasma glucose ≥200 mg/dL (11.1 mmol/L) with classic hyperglycemic symptoms or hyperglycemic crisis**. In the absence of unequivocal symptomatic hyperglycemia, confirm the abnormal result with repeat testing.[1] For many nonpregnant adults, an **A1C target <7%** is appropriate when it can be reached without clinically important hypoglycemia or excessive treatment burden. Targets should be individualized for comorbidity, frailty, function, life expectancy, and hypoglycemia risk. For continuous glucose monitoring (CGM), common goals for many adults are **time 70–180 mg/dL >70%**, **time <70 mg/dL <4%**, and **time <54 mg/dL <1%**.[2] Treatment is no longer a glucose-only ladder. In patients with atherosclerotic cardiovascular disease (ASCVD), heart failure, chronic kidney disease (CKD), obesity, or metabolic liver disease, choose therapies for proven organ benefit even when A1C is close to target.[3-6] Metformin remains effective, inexpensive, and commonly used, but it is not mandatory before therapies with cardiovascular, kidney, or weight benefit. Consider insulin promptly for catabolic symptoms, symptomatic severe hyperglycemia, **A1C >10%**, or **plasma glucose ≥300 mg/dL (16.7 mmol/L)**.[3] In the absence of severe hyperglycemia or crisis, glucagon-like peptide-1 (GLP-1)-based therapy is generally preferred before insulin when an injectable glucose-lowering therapy is needed.[3] Every follow-up should address more than A1C: hypoglycemia, blood pressure, lipids, kidney function and albuminuria, weight, retinopathy, neuropathy and feet, smoking, medication access, and psychosocial barriers all change outcomes. ## Pathophysiology T2D reflects several interacting defects: - **insulin resistance** in skeletal muscle, liver, and adipose tissue; - **progressive beta-cell failure**, with declining ability to compensate for metabolic demand; - excessive hepatic glucose production; - inappropriate glucagon secretion; - altered incretin signaling; - increased renal glucose reabsorption; - adipose inflammation and ectopic fat deposition; - central nervous system changes affecting appetite and energy balance. Hyperglycemia itself worsens beta-cell function and insulin resistance, creating glucotoxicity. Weight loss, improved activity, and effective pharmacotherapy can reduce this burden; substantial sustained weight loss can produce diabetes remission in selected patients, particularly earlier in the disease course.[6] ## Risk factors and screening Risk rises with overweight or obesity, family history, prior gestational diabetes, prediabetes, hypertension, dyslipidemia, polycystic ovary syndrome, physical inactivity, obstructive sleep apnea, metabolic dysfunction-associated steatotic liver disease, and exposure to diabetogenic medications such as glucocorticoids. Screening intervals and starting age vary by jurisdiction and risk profile. Test earlier and more often when risk is high, after gestational diabetes, or when symptoms suggest hyperglycemia.[1] ## Clinical presentation Many patients are asymptomatic and identified by screening. Symptoms can include: - polyuria, polydipsia, and nocturia; - blurred vision; - fatigue; - recurrent genital candidiasis or skin infection; - slow wound healing; - neuropathic symptoms; - unintentional weight loss when hyperglycemia is severe. ### Dangerous presentations | Finding | Main concern | Immediate action | |---|---|---| | Vomiting, abdominal pain, tachypnea, ketosis, acidosis | Diabetic ketoacidosis (DKA), including euglycemic DKA with SGLT2 inhibition | Emergency metabolic workup and DKA pathway | | Severe dehydration, altered mental status, very high glucose/osmolality | Hyperosmolar hyperglycemic state | Emergency fluid/electrolyte management and insulin per crisis protocol | | Glucose <54 mg/dL or event requiring assistance | Clinically significant or severe hypoglycemia | Treat immediately and revise regimen | | New infected foot ulcer, necrosis, spreading cellulitis | Deep infection, osteomyelitis, ischemia | Urgent wound, vascular, and infection assessment | | Acute visual loss or new field defect | Sight-threatening ocular disease | Same-day ophthalmic assessment | | Chest pain, focal neurologic deficit, acute dyspnea | ASCVD event, stroke, or heart failure | Standard emergency pathway | ## Diagnosis ### Diagnostic thresholds in nonpregnant individuals | Test | Diabetes threshold | |---|---:| | A1C | **≥6.5% (48 mmol/mol)** | | Fasting plasma glucose | **≥126 mg/dL (7.0 mmol/L)** after at least 8 hours without caloric intake | | 2-hour plasma glucose during 75-g oral glucose tolerance test | **≥200 mg/dL (11.1 mmol/L)** | | Random plasma glucose | **≥200 mg/dL (11.1 mmol/L)** with classic symptoms or hyperglycemic crisis | Use a validated laboratory method for A1C. When hyperglycemia is not unequivocal, repeat the abnormal test or confirm with another accepted test.[1] ### When A1C is unreliable Prefer plasma glucose-based criteria when red-cell turnover or hemoglobin measurement is substantially altered, including recent blood loss or transfusion, hemolysis, selected hemoglobin variants, erythropoietin therapy, some forms of advanced CKD/anemia, and pregnancy.[1] ### Prediabetes Common ranges are: - A1C **5.7–6.4%**; - fasting plasma glucose **100–125 mg/dL (5.6–6.9 mmol/L)**; - 2-hour 75-g glucose **140–199 mg/dL (7.8–11.0 mmol/L)**.[1] Prediabetes indicates increased diabetes and cardiovascular risk. Management should emphasize weight, activity, sleep, cardiovascular risk reduction, and individualized consideration of preventive pharmacotherapy. ## Confirm that the diabetes type is correct Adults can develop autoimmune diabetes, and T2D can occur in adolescents. Reconsider the classification when there is: - ketosis or DKA at presentation; - rapid progression to insulin dependence; - marked weight loss or a lean phenotype without typical insulin resistance; - personal or family autoimmune disease; - strong multigenerational young-onset diabetes suggesting monogenic disease; - pancreatic disease or pancreatic surgery; - hemochromatosis; - exposure to glucocorticoids, immunotherapy, antipsychotics, or other diabetogenic drugs. Islet autoantibodies and C-peptide can help when classification is uncertain, interpreted in the context of glucose level, treatment, and disease duration.[1] ## Baseline assessment after diagnosis Establish the complication and comorbidity profile early. ### History Assess: - symptoms and likely duration; - prior gestational diabetes or pancreatitis; - diet pattern, activity, sleep, and food insecurity; - weight trajectory; - medication and supplement exposure; - tobacco, alcohol, and substance use; - ASCVD, heart failure, CKD, liver disease, and sleep apnea; - neuropathy, visual symptoms, foot wounds, and sexual dysfunction; - mood, cognition, diabetes distress, and ability to self-manage; - pregnancy plans; - affordability and access barriers. ### Physical assessment Include weight/BMI, blood pressure, cardiovascular status, peripheral pulses, skin and foot integrity, foot sensation, and findings suggesting an alternative endocrine disorder when clinically indicated. ### Common baseline laboratory tests - A1C and plasma glucose; - serum creatinine/eGFR; - urine albumin-to-creatinine ratio (UACR); - lipid profile; - liver biochemistry; - vitamin B12 when deficiency is suspected or after long-term metformin exposure in a patient with anemia or neuropathic symptoms; - other targeted tests according to comorbidity. ## Glycemic targets For many nonpregnant adults, **A1C <7%** is appropriate.[2] Use a lower target only when likely benefit outweighs hypoglycemia and treatment burden. Use a less stringent target when frailty, cognitive impairment, severe comorbidity, recurrent hypoglycemia, or limited life expectancy reduces benefit or increases harm.[2] ### CGM targets for many adults | Metric | Common target | |---|---:| | Time 70–180 mg/dL | **>70%** | | Time <70 mg/dL | **<4%** | | Time <54 mg/dL | **<1%** | | Time >180 mg/dL | **<25%** | | Time >250 mg/dL | **<5%** | Older adults with complex health may need more permissive glucose targets and stricter avoidance of hypoglycemia.[2] ## Lifestyle, weight, and self-management Lifestyle therapy should support rather than delay effective medication. ### Nutrition Use an eating pattern that is culturally appropriate, affordable, and sustainable. Useful principles include: - replace sugar-sweetened beverages and highly refined carbohydrates; - emphasize vegetables, legumes, fiber-rich foods, minimally processed protein sources, and unsaturated fats; - match carbohydrate amount and timing to glucose-lowering therapy when hypoglycemia is possible; - tailor sodium, protein, and potassium advice to kidney and cardiovascular status. ### Physical activity Combine aerobic and resistance activity when feasible, reduce prolonged sedentary time, and adapt activity to cardiovascular disease, neuropathy, retinopathy, foot disease, and musculoskeletal limitations. ### Weight management Weight management is a primary treatment goal when overweight or obesity is present. A sustained **5–7%** weight loss improves glycemia and cardiovascular risk factors; **>10%** often produces larger metabolic benefits and may enable remission in selected patients.[6] When pharmacologic weight treatment is appropriate, agents with high weight-loss efficacy can improve both weight and glycemia. Metabolic surgery is an effective option for selected patients with T2D and obesity; candidacy should follow current multidisciplinary guidance.[6] ## Pharmacologic treatment Therapy should address four parallel goals: 1. glucose control; 2. cardiovascular risk reduction; 3. kidney protection; 4. weight and metabolic benefit. ### Choose by dominant clinical need | Clinical priority | Preferred direction | Key point | |---|---|---| | Established ASCVD or high ASCVD risk | GLP-1 receptor agonist and/or SGLT2 inhibitor with proven cardiovascular benefit | Organ benefit can justify treatment independent of A1C[3] | | Heart failure | SGLT2 inhibitor with proven heart-failure benefit | Benefit extends beyond glucose lowering[3] | | CKD with eGFR ≥20 mL/min/1.73 m² and/or albuminuria | SGLT2 inhibitor with proven kidney benefit; add GLP-1 receptor agonist with proven benefit when appropriate | Glucose-lowering effect of SGLT2 therapy declines at low eGFR, but cardiorenal benefit persists[3,4] | | CKD with eGFR <30 where additional glucose lowering is needed | GLP-1 receptor agonist is generally preferred | Adjust other drugs for renal clearance and hypoglycemia risk[3,4] | | Obesity | Prioritize high-efficacy weight-lowering therapy, especially GLP-1 or dual GIP/GLP-1 pathways when appropriate | Adjust insulin/secretagogues to prevent hypoglycemia[3,6] | | No dominant organ indication | Select among metformin and other agents by efficacy, hypoglycemia risk, weight effect, adverse effects, cost, and preference | Reassess without therapeutic inertia[3] | ### Major glucose-lowering classes | Class | Main advantages | Important limitations/monitoring | |---|---|---| | Metformin | Effective, inexpensive, low hypoglycemia risk, weight neutral/slight loss | GI effects, vitamin B12 deficiency; do not use when eGFR <30; reassess dose/risk as eGFR declines | | SGLT2 inhibitor | Heart-failure and CKD benefit; modest weight loss; low intrinsic hypoglycemia risk | Genital mycotic infection, volume depletion, euglycemic DKA; hold during major surgery/prolonged fasting and significant acute illness according to current label/protocol | | GLP-1 receptor agonist | Strong glucose lowering; weight loss; cardiovascular and kidney benefit with selected agents | GI effects, gallbladder events, rare pancreatitis concern; follow agent-specific contraindications | | Dual GIP/GLP-1 receptor agonist | Very high glucose and weight efficacy | GI effects; titrate gradually; adjust insulin/secretagogues | | DPP-4 inhibitor | Oral, low hypoglycemia risk, weight neutral | Modest efficacy; do not combine with GLP-1 or dual GIP/GLP-1 therapy[3] | | Sulfonylurea | Rapid, inexpensive glucose lowering | Hypoglycemia and weight gain; deintensify when safer therapy can meet goals | | Thiazolidinedione | Insulin sensitization, durable effect in selected patients | Weight gain, edema, heart-failure risk, fractures; agent-specific liver/bladder considerations | | Insulin | Highest glucose-lowering capacity; essential for catabolic/severe hyperglycemia | Hypoglycemia, weight gain, injection burden; requires titration and education | ## When to start insulin Consider insulin promptly when any of the following are present:[3] - catabolic weight loss; - symptomatic severe hyperglycemia; - ketosis; - **A1C >10%**; - **plasma glucose ≥300 mg/dL (16.7 mmol/L)**; - acute illness where noninsulin therapy is insufficient or inappropriate. If severe hyperglycemia or crisis is absent, GLP-1-based therapy is generally preferred before insulin for many patients who need injectable glucose lowering.[3] ### Basal insulin initiation A common starting regimen is **10 units once daily or 0.1–0.2 units/kg/day**, then titrate according to fasting glucose, hypoglycemia, and individualized target.[3] Watch for overbasalization: fasting glucose may be near target while postprandial hyperglycemia persists, with nocturnal hypoglycemia or a large bedtime-to-morning glucose fall. Add therapy addressing postprandial glucose rather than indefinitely escalating basal insulin. ## Chronic kidney disease Measure **UACR and eGFR at least annually in all patients with T2D**. Monitor more often, typically 1–4 times per year depending on CKD stage and treatment, once CKD is present.[4] Kidney-protective care includes: - individualized blood-pressure control; - ACE inhibitor or ARB when indicated for hypertension with albuminuria; - an SGLT2 inhibitor with proven kidney benefit at **eGFR ≥20 mL/min/1.73 m²** when appropriate; - a GLP-1 receptor agonist with demonstrated kidney benefit when indicated; - nonsteroidal mineralocorticoid receptor antagonist therapy in eligible albuminuric CKD with potassium and renal monitoring.[4] Active urine sediment, rapid eGFR decline, abrupt heavy proteinuria, nephrotic syndrome, or atypical systemic findings should prompt consideration of nondiabetic kidney disease and nephrology referral. ## Cardiovascular risk reduction Treat cardiovascular risk with the same intensity as glycemia: - control blood pressure using individualized targets; - prescribe statin therapy according to age and ASCVD risk; - stop tobacco exposure; - use antiplatelet therapy when indicated for established vascular disease, not routinely for every patient with diabetes; - select glucose-lowering therapy with proven ASCVD or heart-failure benefit when the corresponding condition is present.[3] ## Retinopathy, neuropathy, and foot disease ### Retinopathy Because T2D may precede diagnosis by years, arrange a **dilated comprehensive retinal assessment at diagnosis**. If repeated assessments show no retinopathy and glycemia is controlled, a **1–2 year** interval may be considered; established or progressive retinopathy requires at least annual and often more frequent specialist follow-up.[5] Rapid large improvements in glucose can transiently worsen established retinopathy in some patients. Coordinate with ophthalmology when advanced retinopathy is present before major therapy intensification. ### Neuropathy Assess for peripheral neuropathy **at diagnosis and at least annually** thereafter.[5] Screen for symptoms, small- and large-fiber dysfunction, and loss of protective sensation. ### Foot care Perform a comprehensive foot assessment at least annually, including skin, deformity, pulses, and **10-g monofilament** testing plus another sensory modality. Inspect the feet at every visit in patients with prior ulcer/amputation or established loss of protective sensation.[5] New ulceration, infection, necrosis, or ischemic change requires prompt multidisciplinary management. See [Diabetes-Related Foot Infection](../infectious-disease/diabetes-related-foot-infection.md). ## Hypoglycemia Hypoglycemia is driven mainly by insulin, sulfonylureas, and meglitinides. | Level | Definition | |---|---| | 1 | Glucose **<70 mg/dL and ≥54 mg/dL** | | 2 | Glucose **<54 mg/dL** | | 3 | Severe event requiring assistance, regardless of measured glucose | For a conscious patient with glucose <70 mg/dL, give rapidly absorbed glucose/carbohydrate and reassess promptly. Prescribe glucagon for patients at high risk and train family/caregivers when appropriate.[2] After level 2 or 3 hypoglycemia, actively revise therapy. Review kidney function, nutrition, alcohol, exercise, cognition, medication interactions, food access, and glycemic targets. Deintensify insulin or secretagogues when the harm exceeds benefit.[2] ## Sick-day and perioperative care Acute illness can cause hyperglycemia, ketosis, dehydration, or hypoglycemia. - Maintain hydration when possible. - Monitor glucose more often; check ketones when ketosis is plausible. - Do not stop basal insulin in insulin-deficient patients. - Temporarily hold SGLT2 inhibitors during major surgery, prolonged fasting, or acute illness associated with reduced intake, dehydration, or ketoacidosis risk, following the current product label and local perioperative protocol.[3] - Hold metformin during significant hypoxia, shock, severe AKI, or other conditions that materially increase lactic-acidosis risk; restart when the acute risk has resolved and renal function is appropriate. Nausea, abdominal pain, tachypnea, or malaise in a patient taking an SGLT2 inhibitor should trigger evaluation for **euglycemic DKA even when glucose is not markedly elevated**. ## Monitoring schedule | Item | Typical interval | |---|---| | A1C | About every 3 months while therapy is changing or goal is not met; less often when stable | | CGM/glucose data | At treatment review when used, with more frequent review after dose changes or hypoglycemia | | Blood pressure | Routine visits | | Lipids | At diagnosis and according to lipid therapy/risk | | eGFR + UACR | At least annually; 1–4 times/year with CKD according to stage[4] | | Retinal assessment | At diagnosis; then based on findings, commonly annually or every 1–2 years if repeatedly normal and controlled[5] | | Neuropathy/foot assessment | At least annually; every visit for high-risk feet[5] | | Weight/BMI | Routine care; at least every 3 months during active weight treatment[6] | | Hypoglycemia history | Every encounter when risk is present[2] | ## Management pathway ```text Confirmed T2D | v Classify correctly: any ketosis, weight loss, autoimmune or monogenic clues? | v Map major risks: ASCVD | heart failure | CKD/UACR | obesity | liver disease | hypoglycemia | frailty | access | +--> Catabolic symptoms / A1C >10% / glucose >=300 mg/dL / ketosis? | | | +--> Consider insulin promptly; evaluate for hyperglycemic crisis | v Lifestyle + weight treatment + glucose-lowering therapy | +--> ASCVD: proven GLP-1 and/or SGLT2 cardiovascular benefit +--> Heart failure: proven SGLT2 benefit +--> CKD: SGLT2 if eGFR >=20 when appropriate; add proven GLP-1 pathway as indicated +--> Obesity: prioritize high-efficacy weight-benefit therapy +--> No dominant organ indication: choose by efficacy, safety, weight, cost, preference | v Reassess A1C/CGM, hypoglycemia, kidney function, weight, complications, adherence | +--> At goal and safe: maintain +--> Not at goal: intensify or change therapy without delay +--> Hypoglycemia/treatment burden: deintensify high-risk therapy ``` ## Special populations ### Older adults and frailty Prioritize avoidance of hypoglycemia, simple regimens, cognition and dexterity, fall risk, renal function, caregiver capacity, and medication burden. Deintensification is appropriate when treatment harms exceed likely benefit.[2] ### Pregnancy Preexisting T2D in pregnancy requires specialist care. Glucose targets and medication safety differ substantially from routine adult care. Insulin is commonly required; many noninsulin glucose-lowering agents, renin-angiotensin system blockers, statins, and weight-loss drugs require discontinuation or substitution. Preconception care should include medication review, retinal assessment, folate, and optimization of glycemia before conception where feasible. ### Cost-limited care Assess affordability directly. Lower-cost metformin, sulfonylureas, thiazolidinediones, and human insulin may be necessary, but hypoglycemia, weight gain, and monitoring burden must be incorporated into the decision. Access limitations should not be mistaken for nonadherence. ## Complications and prevention | Complication | Detection | Prevention/management priority | |---|---|---| | Retinopathy | Retinal assessment | Glycemic and blood-pressure control; ophthalmic treatment when indicated | | CKD | UACR + eGFR | RAAS blockade when indicated, SGLT2/GLP-1 kidney benefit, potassium monitoring | | Neuropathy | Symptoms + sensory testing | Glycemic optimization, foot protection, pain treatment | | Foot ulcer/amputation | Skin/pulse/sensation assessment | Protective footwear/offloading, vascular review, infection treatment | | ASCVD | Global risk assessment | Statin, blood pressure control, tobacco cessation, proven organ-benefit therapies | | Heart failure | Dyspnea, edema, congestion | SGLT2 therapy plus standard heart-failure care | | Hypoglycemia | Active history/CGM | Deintensify insulin/secretagogues, glucagon, education | | Metabolic liver disease | Fibrosis-risk assessment when indicated | Weight loss and therapies with metabolic/liver benefit | ## Current practice changes The 2026 Standards of Care reinforce several shifts:[2-6] - organ protection can determine drug choice independently of A1C; - GLP-1-based therapy is preferred before insulin for many adults who need injectable treatment but do not have severe hyperglycemia or crisis; - kidney protection uses both SGLT2 and GLP-1 pathways according to eGFR, albuminuria, and comorbidity; - CGM is increasingly used beyond intensive insulin regimens when it materially improves safety or management; - obesity is treated as a chronic disease and a primary therapeutic target, not merely a lifestyle adjunct; - deintensification is an active safety intervention when hypoglycemia or treatment burden outweighs benefit. ## Related library topics - [Diabetic Ketoacidosis](diabetic-ketoacidosis.md) - [Chronic Kidney Disease](../nephrology/chronic-kidney-disease.md) - [Dyslipidemia in Adults](../cardiology/dyslipidemia-in-adults.md) - [Obesity in Adults](obesity-in-adults.md) - [Diabetic Retinopathy and Diabetic Macular Edema](../ophthalmology/diabetic-retinopathy-and-diabetic-macular-edema.md) - [Diabetes-Related Foot Infection](../infectious-disease/diabetes-related-foot-infection.md) ## References 1. American Diabetes Association Professional Practice Committee. 2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S27-S49. DOI: 10.2337/dc26-S002. https://diabetesjournals.org/care/article/49/Supplement_1/S27/163920/2-Diagnosis-and-Classification-of-Diabetes 2. American Diabetes Association Professional Practice Committee. 6. Glycemic Goals, Hypoglycemia, and Hyperglycemic Crises: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S132-S149. DOI: 10.2337/dc26-S006. https://diabetesjournals.org/care/article/49/Supplement_1/S132/163927/6-Glycemic-Goals-Hypoglycemia-and-Hyperglycemic 3. American Diabetes Association Professional Practice Committee. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S183-S215. DOI: 10.2337/dc26-S009. https://doi.org/10.2337/dc26-S009 4. American Diabetes Association Professional Practice Committee. 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S246-S260. DOI: 10.2337/dc26-S011. https://doi.org/10.2337/dc26-S011 5. American Diabetes Association Professional Practice Committee. 12. Retinopathy, Neuropathy, and Foot Care: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S261-S276. DOI: 10.2337/dc26-S012. PMID: 41358886. https://doi.org/10.2337/dc26-S012 6. American Diabetes Association Professional Practice Committee. 8. Obesity and Weight Management for the Prevention and Treatment of Diabetes: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S166-S182. DOI: 10.2337/dc26-S008. https://doi.org/10.2337/dc26-S00819:T6321,## Summary Type 2 diabetes mellitus (T2D) is chronic hyperglycemia caused by progressive beta-cell dysfunction on a background of insulin resistance and broader metabolic dysregulation. Diagnosis in a nonpregnant person is established by **A1C ≥6.5% (48 mmol/mol)**, **fasting plasma glucose ≥126 mg/dL (7.0 mmol/L)**, **2-hour plasma glucose ≥200 mg/dL (11.1 mmol/L) during a 75-g oral glucose tolerance test**, or **random plasma glucose ≥200 mg/dL (11.1 mmol/L) with classic hyperglycemic symptoms or hyperglycemic crisis**. In the absence of unequivocal symptomatic hyperglycemia, confirm the abnormal result with repeat testing.[1] For many nonpregnant adults, an **A1C target <7%** is appropriate when it can be reached without clinically important hypoglycemia or excessive treatment burden. Targets should be individualized for comorbidity, frailty, function, life expectancy, and hypoglycemia risk. For continuous glucose monitoring (CGM), common goals for many adults are **time 70–180 mg/dL >70%**, **time <70 mg/dL <4%**, and **time <54 mg/dL <1%**.[2] Treatment is no longer a glucose-only ladder. In patients with atherosclerotic cardiovascular disease (ASCVD), heart failure, chronic kidney disease (CKD), obesity, or metabolic liver disease, choose therapies for proven organ benefit even when A1C is close to target.[3-6] Metformin remains effective, inexpensive, and commonly used, but it is not mandatory before therapies with cardiovascular, kidney, or weight benefit. Consider insulin promptly for catabolic symptoms, symptomatic severe hyperglycemia, **A1C >10%**, or **plasma glucose ≥300 mg/dL (16.7 mmol/L)**.[3] In the absence of severe hyperglycemia or crisis, glucagon-like peptide-1 (GLP-1)-based therapy is generally preferred before insulin when an injectable glucose-lowering therapy is needed.[3] Every follow-up should address more than A1C: hypoglycemia, blood pressure, lipids, kidney function and albuminuria, weight, retinopathy, neuropathy and feet, smoking, medication access, and psychosocial barriers all change outcomes. ## Pathophysiology T2D reflects several interacting defects: - **insulin resistance** in skeletal muscle, liver, and adipose tissue; - **progressive beta-cell failure**, with declining ability to compensate for metabolic demand; - excessive hepatic glucose production; - inappropriate glucagon secretion; - altered incretin signaling; - increased renal glucose reabsorption; - adipose inflammation and ectopic fat deposition; - central nervous system changes affecting appetite and energy balance. Hyperglycemia itself worsens beta-cell function and insulin resistance, creating glucotoxicity. Weight loss, improved activity, and effective pharmacotherapy can reduce this burden; substantial sustained weight loss can produce diabetes remission in selected patients, particularly earlier in the disease course.[6] ## Risk factors and screening Risk rises with overweight or obesity, family history, prior gestational diabetes, prediabetes, hypertension, dyslipidemia, polycystic ovary syndrome, physical inactivity, obstructive sleep apnea, metabolic dysfunction-associated steatotic liver disease, and exposure to diabetogenic medications such as glucocorticoids. Screening intervals and starting age vary by jurisdiction and risk profile. Test earlier and more often when risk is high, after gestational diabetes, or when symptoms suggest hyperglycemia.[1] ## Clinical presentation Many patients are asymptomatic and identified by screening. Symptoms can include: - polyuria, polydipsia, and nocturia; - blurred vision; - fatigue; - recurrent genital candidiasis or skin infection; - slow wound healing; - neuropathic symptoms; - unintentional weight loss when hyperglycemia is severe. ### Dangerous presentations | Finding | Main concern | Immediate action | |---|---|---| | Vomiting, abdominal pain, tachypnea, ketosis, acidosis | [Diabetic ketoacidosis](/library/diabetic-ketoacidosis) (DKA), including euglycemic DKA with SGLT2 inhibition | Emergency metabolic workup and DKA pathway | | Severe dehydration, altered mental status, very high glucose/osmolality | Hyperosmolar hyperglycemic state | Emergency fluid/electrolyte management and insulin per crisis protocol | | Glucose <54 mg/dL or event requiring assistance | Clinically significant or severe hypoglycemia | Treat immediately and revise regimen | | New infected foot ulcer, necrosis, spreading cellulitis | Deep infection, osteomyelitis, ischemia | Urgent wound, vascular, and infection assessment | | Acute visual loss or new field defect | Sight-threatening ocular disease | Same-day ophthalmic assessment | | Chest pain, focal neurologic deficit, acute dyspnea | ASCVD event, stroke, or heart failure | Standard emergency pathway | ## Diagnosis ### Diagnostic thresholds in nonpregnant individuals | Test | Diabetes threshold | |---|---:| | A1C | **≥6.5% (48 mmol/mol)** | | Fasting plasma glucose | **≥126 mg/dL (7.0 mmol/L)** after at least 8 hours without caloric intake | | 2-hour plasma glucose during 75-g oral glucose tolerance test | **≥200 mg/dL (11.1 mmol/L)** | | Random plasma glucose | **≥200 mg/dL (11.1 mmol/L)** with classic symptoms or hyperglycemic crisis | Use a validated laboratory method for A1C. When hyperglycemia is not unequivocal, repeat the abnormal test or confirm with another accepted test.[1] ### When A1C is unreliable Prefer plasma glucose-based criteria when red-cell turnover or hemoglobin measurement is substantially altered, including recent blood loss or transfusion, hemolysis, selected hemoglobin variants, erythropoietin therapy, some forms of advanced CKD/anemia, and pregnancy.[1] ### Prediabetes Common ranges are: - A1C **5.7–6.4%**; - fasting plasma glucose **100–125 mg/dL (5.6–6.9 mmol/L)**; - 2-hour 75-g glucose **140–199 mg/dL (7.8–11.0 mmol/L)**.[1] Prediabetes indicates increased diabetes and cardiovascular risk. Management should emphasize weight, activity, sleep, cardiovascular risk reduction, and individualized consideration of preventive pharmacotherapy. ## Confirm that the diabetes type is correct Adults can develop autoimmune diabetes, and T2D can occur in adolescents. Reconsider the classification when there is: - ketosis or DKA at presentation; - rapid progression to insulin dependence; - marked weight loss or a lean phenotype without typical insulin resistance; - personal or family autoimmune disease; - strong multigenerational young-onset diabetes suggesting monogenic disease; - pancreatic disease or pancreatic surgery; - hemochromatosis; - exposure to glucocorticoids, immunotherapy, antipsychotics, or other diabetogenic drugs. Islet autoantibodies and C-peptide can help when classification is uncertain, interpreted in the context of glucose level, treatment, and disease duration.[1] ## Baseline assessment after diagnosis Establish the complication and comorbidity profile early. ### History Assess: - symptoms and likely duration; - prior gestational diabetes or pancreatitis; - diet pattern, activity, sleep, and food insecurity; - weight trajectory; - medication and supplement exposure; - tobacco, alcohol, and substance use; - ASCVD, heart failure, CKD, liver disease, and sleep apnea; - neuropathy, visual symptoms, foot wounds, and sexual dysfunction; - mood, cognition, diabetes distress, and ability to self-manage; - pregnancy plans; - affordability and access barriers. ### Physical assessment Include weight/BMI, blood pressure, cardiovascular status, peripheral pulses, skin and foot integrity, foot sensation, and findings suggesting an alternative endocrine disorder when clinically indicated. ### Common baseline laboratory tests - A1C and plasma glucose; - serum creatinine/eGFR; - urine albumin-to-creatinine ratio (UACR); - lipid profile; - liver biochemistry; - vitamin B12 when deficiency is suspected or after long-term metformin exposure in a patient with anemia or neuropathic symptoms; - other targeted tests according to comorbidity. ## Glycemic targets For many nonpregnant adults, **A1C <7%** is appropriate.[2] Use a lower target only when likely benefit outweighs hypoglycemia and treatment burden. Use a less stringent target when frailty, cognitive impairment, severe comorbidity, recurrent hypoglycemia, or limited life expectancy reduces benefit or increases harm.[2] ### CGM targets for many adults | Metric | Common target | |---|---:| | Time 70–180 mg/dL | **>70%** | | Time <70 mg/dL | **<4%** | | Time <54 mg/dL | **<1%** | | Time >180 mg/dL | **<25%** | | Time >250 mg/dL | **<5%** | Older adults with complex health may need more permissive glucose targets and stricter avoidance of hypoglycemia.[2] ## Lifestyle, weight, and self-management Lifestyle therapy should support rather than delay effective medication. ### Nutrition Use an eating pattern that is culturally appropriate, affordable, and sustainable. Useful principles include: - replace sugar-sweetened beverages and highly refined carbohydrates; - emphasize vegetables, legumes, fiber-rich foods, minimally processed protein sources, and unsaturated fats; - match carbohydrate amount and timing to glucose-lowering therapy when hypoglycemia is possible; - tailor sodium, protein, and potassium advice to kidney and cardiovascular status. ### Physical activity Combine aerobic and resistance activity when feasible, reduce prolonged sedentary time, and adapt activity to cardiovascular disease, neuropathy, retinopathy, foot disease, and musculoskeletal limitations. ### Weight management Weight management is a primary treatment goal when overweight or obesity is present. A sustained **5–7%** weight loss improves glycemia and cardiovascular risk factors; **>10%** often produces larger metabolic benefits and may enable remission in selected patients.[6] When pharmacologic weight treatment is appropriate, agents with high weight-loss efficacy can improve both weight and glycemia. Metabolic surgery is an effective option for selected patients with T2D and obesity; candidacy should follow current multidisciplinary guidance.[6] ## Pharmacologic treatment Therapy should address four parallel goals: 1. glucose control; 2. cardiovascular risk reduction; 3. kidney protection; 4. weight and metabolic benefit. ### Choose by dominant clinical need | Clinical priority | Preferred direction | Key point | |---|---|---| | Established ASCVD or high ASCVD risk | GLP-1 receptor agonist and/or SGLT2 inhibitor with proven cardiovascular benefit | Organ benefit can justify treatment independent of A1C[3] | | Heart failure | SGLT2 inhibitor with proven heart-failure benefit | Benefit extends beyond glucose lowering[3] | | CKD with eGFR ≥20 mL/min/1.73 m² and/or albuminuria | SGLT2 inhibitor with proven kidney benefit; add GLP-1 receptor agonist with proven benefit when appropriate | Glucose-lowering effect of SGLT2 therapy declines at low eGFR, but cardiorenal benefit persists[3,4] | | CKD with eGFR <30 where additional glucose lowering is needed | GLP-1 receptor agonist is generally preferred | Adjust other drugs for renal clearance and hypoglycemia risk[3,4] | | Obesity | Prioritize high-efficacy weight-lowering therapy, especially GLP-1 or dual GIP/GLP-1 pathways when appropriate | Adjust insulin/secretagogues to prevent hypoglycemia[3,6] | | No dominant organ indication | Select among metformin and other agents by efficacy, hypoglycemia risk, weight effect, adverse effects, cost, and preference | Reassess without therapeutic inertia[3] | ### Major glucose-lowering classes | Class | Main advantages | Important limitations/monitoring | |---|---|---| | Metformin | Effective, inexpensive, low hypoglycemia risk, weight neutral/slight loss | GI effects, vitamin B12 deficiency; do not use when eGFR <30; reassess dose/risk as eGFR declines | | SGLT2 inhibitor | Heart-failure and CKD benefit; modest weight loss; low intrinsic hypoglycemia risk | Genital mycotic infection, volume depletion, euglycemic DKA; hold during major surgery/prolonged fasting and significant acute illness according to current label/protocol | | GLP-1 receptor agonist | Strong glucose lowering; weight loss; cardiovascular and kidney benefit with selected agents | GI effects, gallbladder events, rare pancreatitis concern; follow agent-specific contraindications | | Dual GIP/GLP-1 receptor agonist | Very high glucose and weight efficacy | GI effects; titrate gradually; adjust insulin/secretagogues | | DPP-4 inhibitor | Oral, low hypoglycemia risk, weight neutral | Modest efficacy; do not combine with GLP-1 or dual GIP/GLP-1 therapy[3] | | Sulfonylurea | Rapid, inexpensive glucose lowering | Hypoglycemia and weight gain; deintensify when safer therapy can meet goals | | Thiazolidinedione | Insulin sensitization, durable effect in selected patients | Weight gain, edema, heart-failure risk, fractures; agent-specific liver/bladder considerations | | Insulin | Highest glucose-lowering capacity; essential for catabolic/severe hyperglycemia | Hypoglycemia, weight gain, injection burden; requires titration and education | ## When to start insulin Consider insulin promptly when any of the following are present:[3] - catabolic weight loss; - symptomatic severe hyperglycemia; - ketosis; - **A1C >10%**; - **plasma glucose ≥300 mg/dL (16.7 mmol/L)**; - acute illness where noninsulin therapy is insufficient or inappropriate. If severe hyperglycemia or crisis is absent, GLP-1-based therapy is generally preferred before insulin for many patients who need injectable glucose lowering.[3] ### Basal insulin initiation A common starting regimen is **10 units once daily or 0.1–0.2 units/kg/day**, then titrate according to fasting glucose, hypoglycemia, and individualized target.[3] Watch for overbasalization: fasting glucose may be near target while postprandial hyperglycemia persists, with nocturnal hypoglycemia or a large bedtime-to-morning glucose fall. Add therapy addressing postprandial glucose rather than indefinitely escalating basal insulin. ## Chronic kidney disease Measure **UACR and eGFR at least annually in all patients with T2D**. Monitor more often, typically 1–4 times per year depending on CKD stage and treatment, once CKD is present.[4] Kidney-protective care includes: - individualized blood-pressure control; - ACE inhibitor or ARB when indicated for hypertension with albuminuria; - an SGLT2 inhibitor with proven kidney benefit at **eGFR ≥20 mL/min/1.73 m²** when appropriate; - a GLP-1 receptor agonist with demonstrated kidney benefit when indicated; - nonsteroidal mineralocorticoid receptor antagonist therapy in eligible albuminuric CKD with potassium and renal monitoring.[4] Active urine sediment, rapid eGFR decline, abrupt heavy proteinuria, nephrotic syndrome, or atypical systemic findings should prompt consideration of nondiabetic kidney disease and nephrology referral. ## Cardiovascular risk reduction Treat cardiovascular risk with the same intensity as glycemia: - control blood pressure using individualized targets; - prescribe statin therapy according to age and ASCVD risk; - stop tobacco exposure; - use antiplatelet therapy when indicated for established vascular disease, not routinely for every patient with diabetes; - select glucose-lowering therapy with proven ASCVD or heart-failure benefit when the corresponding condition is present.[3] ## Retinopathy, neuropathy, and foot disease ### Retinopathy Because T2D may precede diagnosis by years, arrange a **dilated comprehensive retinal assessment at diagnosis**. If repeated assessments show no retinopathy and glycemia is controlled, a **1–2 year** interval may be considered; established or progressive retinopathy requires at least annual and often more frequent specialist follow-up.[5] Rapid large improvements in glucose can transiently worsen established retinopathy in some patients. Coordinate with ophthalmology when advanced retinopathy is present before major therapy intensification. ### Neuropathy Assess for peripheral neuropathy **at diagnosis and at least annually** thereafter.[5] Screen for symptoms, small- and large-fiber dysfunction, and loss of protective sensation. ### Foot care Perform a comprehensive foot assessment at least annually, including skin, deformity, pulses, and **10-g monofilament** testing plus another sensory modality. Inspect the feet at every visit in patients with prior ulcer/amputation or established loss of protective sensation.[5] New ulceration, infection, necrosis, or ischemic change requires prompt multidisciplinary management. See [Diabetes-Related Foot Infection](../infectious-disease/diabetes-related-foot-infection.md). ## Hypoglycemia Hypoglycemia is driven mainly by insulin, sulfonylureas, and meglitinides. | Level | Definition | |---|---| | 1 | Glucose **<70 mg/dL and ≥54 mg/dL** | | 2 | Glucose **<54 mg/dL** | | 3 | Severe event requiring assistance, regardless of measured glucose | For a conscious patient with glucose <70 mg/dL, give rapidly absorbed glucose/carbohydrate and reassess promptly. Prescribe glucagon for patients at high risk and train family/caregivers when appropriate.[2] After level 2 or 3 hypoglycemia, actively revise therapy. Review kidney function, nutrition, alcohol, exercise, cognition, medication interactions, food access, and glycemic targets. Deintensify insulin or secretagogues when the harm exceeds benefit.[2] ## Sick-day and perioperative care Acute illness can cause hyperglycemia, ketosis, dehydration, or hypoglycemia. - Maintain hydration when possible. - Monitor glucose more often; check ketones when ketosis is plausible. - Do not stop basal insulin in insulin-deficient patients. - Temporarily hold SGLT2 inhibitors during major surgery, prolonged fasting, or acute illness associated with reduced intake, dehydration, or ketoacidosis risk, following the current product label and local perioperative protocol.[3] - Hold metformin during significant hypoxia, shock, severe AKI, or other conditions that materially increase lactic-acidosis risk; restart when the acute risk has resolved and renal function is appropriate. Nausea, abdominal pain, tachypnea, or malaise in a patient taking an SGLT2 inhibitor should trigger evaluation for **euglycemic DKA even when glucose is not markedly elevated**. ## Monitoring schedule | Item | Typical interval | |---|---| | A1C | About every 3 months while therapy is changing or goal is not met; less often when stable | | CGM/glucose data | At treatment review when used, with more frequent review after dose changes or hypoglycemia | | Blood pressure | Routine visits | | Lipids | At diagnosis and according to lipid therapy/risk | | eGFR + UACR | At least annually; 1–4 times/year with CKD according to stage[4] | | Retinal assessment | At diagnosis; then based on findings, commonly annually or every 1–2 years if repeatedly normal and controlled[5] | | Neuropathy/foot assessment | At least annually; every visit for high-risk feet[5] | | Weight/BMI | Routine care; at least every 3 months during active weight treatment[6] | | Hypoglycemia history | Every encounter when risk is present[2] | ## Management pathway ```text Confirmed T2D | v Classify correctly: any ketosis, weight loss, autoimmune or monogenic clues? | v Map major risks: ASCVD | heart failure | CKD/UACR | obesity | liver disease | hypoglycemia | frailty | access | +--> Catabolic symptoms / A1C >10% / glucose >=300 mg/dL / ketosis? | | | +--> Consider insulin promptly; evaluate for hyperglycemic crisis | v Lifestyle + weight treatment + glucose-lowering therapy | +--> ASCVD: proven GLP-1 and/or SGLT2 cardiovascular benefit +--> Heart failure: proven SGLT2 benefit +--> CKD: SGLT2 if eGFR >=20 when appropriate; add proven GLP-1 pathway as indicated +--> Obesity: prioritize high-efficacy weight-benefit therapy +--> No dominant organ indication: choose by efficacy, safety, weight, cost, preference | v Reassess A1C/CGM, hypoglycemia, kidney function, weight, complications, adherence | +--> At goal and safe: maintain +--> Not at goal: intensify or change therapy without delay +--> Hypoglycemia/treatment burden: deintensify high-risk therapy ``` ## Special populations ### Older adults and frailty Prioritize avoidance of hypoglycemia, simple regimens, cognition and dexterity, fall risk, renal function, caregiver capacity, and medication burden. Deintensification is appropriate when treatment harms exceed likely benefit.[2] ### Pregnancy Preexisting T2D in pregnancy requires specialist care. Glucose targets and medication safety differ substantially from routine adult care. Insulin is commonly required; many noninsulin glucose-lowering agents, renin-angiotensin system blockers, statins, and weight-loss drugs require discontinuation or substitution. Preconception care should include medication review, retinal assessment, folate, and optimization of glycemia before conception where feasible. ### Cost-limited care Assess affordability directly. Lower-cost metformin, sulfonylureas, thiazolidinediones, and human insulin may be necessary, but hypoglycemia, weight gain, and monitoring burden must be incorporated into the decision. Access limitations should not be mistaken for nonadherence. ## Complications and prevention | Complication | Detection | Prevention/management priority | |---|---|---| | Retinopathy | Retinal assessment | Glycemic and blood-pressure control; ophthalmic treatment when indicated | | CKD | UACR + eGFR | RAAS blockade when indicated, SGLT2/GLP-1 kidney benefit, potassium monitoring | | Neuropathy | Symptoms + sensory testing | Glycemic optimization, foot protection, pain treatment | | Foot ulcer/amputation | Skin/pulse/sensation assessment | Protective footwear/offloading, vascular review, infection treatment | | ASCVD | Global risk assessment | Statin, blood pressure control, tobacco cessation, proven organ-benefit therapies | | Heart failure | Dyspnea, edema, congestion | SGLT2 therapy plus standard heart-failure care | | Hypoglycemia | Active history/CGM | Deintensify insulin/secretagogues, glucagon, education | | Metabolic liver disease | Fibrosis-risk assessment when indicated | Weight loss and therapies with metabolic/liver benefit | ## Current practice changes The 2026 Standards of Care reinforce several shifts:[2-6] - organ protection can determine drug choice independently of A1C; - GLP-1-based therapy is preferred before insulin for many adults who need injectable treatment but do not have severe hyperglycemia or crisis; - kidney protection uses both SGLT2 and GLP-1 pathways according to eGFR, albuminuria, and comorbidity; - CGM is increasingly used beyond intensive insulin regimens when it materially improves safety or management; - obesity is treated as a chronic disease and a primary therapeutic target, not merely a lifestyle adjunct; - deintensification is an active safety intervention when hypoglycemia or treatment burden outweighs benefit. ## Related library topics - [Diabetic Ketoacidosis](diabetic-ketoacidosis.md) - [Chronic Kidney Disease](../nephrology/chronic-kidney-disease.md) - [Dyslipidemia in Adults](../cardiology/dyslipidemia-in-adults.md) - [Obesity in Adults](obesity-in-adults.md) - [Diabetic Retinopathy and Diabetic Macular Edema](../ophthalmology/diabetic-retinopathy-and-diabetic-macular-edema.md) - [Diabetes-Related Foot Infection](../infectious-disease/diabetes-related-foot-infection.md) ## References 1. American Diabetes Association Professional Practice Committee. 2. Diagnosis and Classification of Diabetes: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S27-S49. DOI: 10.2337/dc26-S002. https://diabetesjournals.org/care/article/49/Supplement_1/S27/163920/2-Diagnosis-and-Classification-of-Diabetes 2. American Diabetes Association Professional Practice Committee. 6. Glycemic Goals, Hypoglycemia, and Hyperglycemic Crises: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S132-S149. DOI: 10.2337/dc26-S006. https://diabetesjournals.org/care/article/49/Supplement_1/S132/163927/6-Glycemic-Goals-Hypoglycemia-and-Hyperglycemic 3. American Diabetes Association Professional Practice Committee. 9. Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S183-S215. DOI: 10.2337/dc26-S009. https://doi.org/10.2337/dc26-S009 4. American Diabetes Association Professional Practice Committee. 11. Chronic Kidney Disease and Risk Management: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S246-S260. DOI: 10.2337/dc26-S011. https://doi.org/10.2337/dc26-S011 5. American Diabetes Association Professional Practice Committee. 12. Retinopathy, Neuropathy, and Foot Care: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S261-S276. DOI: 10.2337/dc26-S012. PMID: 41358886. https://doi.org/10.2337/dc26-S012 6. American Diabetes Association Professional Practice Committee. 8. Obesity and Weight Management for the Prevention and Treatment of Diabetes: Standards of Care in Diabetes—2026. *Diabetes Care*. 2026;49(Suppl 1):S166-S182. DOI: 10.2337/dc26-S008. https://doi.org/10.2337/dc26-S0087:["$","$L17",null,{"article":{"id":"medical-type-2-diabetes-mellitus","title":"Type 2 Diabetes Mellitus","slug":"type-2-diabetes-mellitus","description":"Type 2 diabetes mellitus (T2D) is chronic hyperglycemia caused by progressive beta-cell dysfunction on a background of insulin resistance and broader metabolic dysregulation. 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