Cortisol.

Glucagon.

Growth hormone.

Insulin.

Epinephrine.

GLP-1 agonists.

Sulfonylureas.

DPP-4 inhibitors.

Thiazolidinediones.

Biguanides.

Blocking renal glucose reabsorption.

Increasing insulin secretion.

Delaying gastric emptying.

Enhancing peripheral GLUT-4 activity.

Inhibiting hepatic glucose production.

Decreased β-cell mass due to aging; typically presents with obesity and normal insulin levels.

Environmental toxins triggering α-cell hyperactivity lead to chronic hypoglycemia.

Insulin resistance in peripheral tissues leads to mild hyperglycemia without ketosis.

Genetic defects in GLUT-4 transporters cause gestational hyperglycemia during pregnancy.

Autoimmune destruction of β-cells causing absolute insulin deficiency; results in polydipsia, polyphagia, polyuria, weight loss, and ketoacidosis.

Type 1: 90%–95% prevalence, onset over age 35, strong genetic predisposition with β-cell insulin production inability.

Type 1: 5%–10% prevalence, undernourished at onset, β-cells destroyed, eliminating insulin production.

Both types: Equal prevalence, similar onset age, shared absolute insulin deficiency.

Type 2: 5%–10% prevalence, onset in childhood/puberty, moderate genetic link with autoimmune β-cell destruction.

Type 2: Onset during puberty, absent obesity, defect in insulin resistance without β-cell decline.

Recombinant human insulin via E. coli/yeast; subcutaneous injection preferred, IV for emergencies, pump for basal/bolus delivery; onset/duration varies by preparation.

Inhaled form only for Type 2; hepatic extraction makes C-peptide irrelevant.

Produced via oral tablets; degraded by insulin protease in the GI tract for rapid absorption.

Degraded minimally in the kidney; contraindicated in renal insufficiency without dose adjustment.

Long-acting only; physical activity shortens duration without site rotation.

Stimulated by epinephrine during fasting; impaired by genetic GLUT defects.

Increased blood glucose uptake via GLUT transporters, metabolized to ATP, blocking K⁺ channels, depolarizing the membrane, Ca²⁺ influx, and exocytosis; impaired by absolute β-cell loss.

Triggered by low ATP, blocking Ca²⁺ influx; impaired due to excess proinsulin cleavage.

Regulated solely by amino acids; impaired in obesity-related resistance.

Inhibited by somatostatin on voltage-gated channels; impaired by viral triggers only.

Sulfonylureas; bind ATP-dependent K⁺ channels on β-cells for insulin secretion.

Alpha-glucosidase inhibitors (e.g., Acarbose); delay carbohydrate digestion in the intestine.

GLP-1 agonists (e.g., Semaglutide); delay gastric emptying and inhibit glucagon.

SGLT-2 inhibitors (e.g., Empagliflozin); promote urinary glucose excretion for CV benefits.

Biguanides (e.g., Metformin); first-line therapy, also used off-label for PCOS and weight reduction.

Gamma (γ) cells.

Delta (δ) cells.

Beta (β) cells.

Epsilon (ε) cells.

Alpha (α) cells.

Activate PPAR-γ for lipid/glucose gene modulation; used in dual PPAR agonists like Saroglitazar.

Bind ATP-dependent K⁺ channels on β-cells, depolarize to increase Ca²⁺ and insulin secretion; long duration (~24 hours).

Inhibit DPP-4 to increase incretin levels; short duration (~12 hours).

Inhibit α-amylase for delayed sugar breakdown; first-line for gestational diabetes.

Block SGLT-2 in kidneys for 90% glucose reabsorption inhibition; beneficial in heart/kidney disease.