Insulin and hypoglycemic drugs

Insulin and hypoglycemic drugs

Diabetes mellitus

·         It is chronic metabolic disorder characterized by a high blood glucose concentration (Hyperglycemia).


Type-I diabetes

Type-II diabetes

·         Body no longer able to produce insulin.

·         Usually develops during childhood, but develops at any age.

·         Still producing insulin, but it does not make enough.

·         Can develops at any age but is most common in adults over age 45.


·         Family history

·         Overweight, high blood pressure etc.


·         Blurry vision

·         Frequent urination

·         Increase appetite and thirst

·         Mood changes

·         Tiredness and weakness

·         Unexpected weight loss

·         Blurry vision

·         Frequent urination

·         Increase appetite and thirst

·         Mood changes

·         Tiredness and weakness

·         Unexpected weight loss


·         No known prevention methods

·         Healthy lifestyle


·         Insulin injection

·         Healthy living



·         Pancreas is the second largest gland of the human body lies in the abdomen behind the stomach and it plays an important role in maintaining sugar level.

·         Pancreas has exocrine as well as endocrine function.

·         Exocrine: secrete enzyme that help with digestion.

·         Endocrine: hormone secreted to the blood by endocrine gland of the pancreas maintain blood glucose level.

·         99% of the pancreatic mass concerned with exocrine and about 1% mass concerned with endocrine system.

·         The Acinar cell of the pancreas is the functional unit of the exocrine.

·         It synthesizes, stores, and secretes digestive enzymes which are activated when it reached to the duodenum.

·         The endocrine system of the pancreas composed of cluster of cells called “Islet of Langerhans”.

·         Pancreatic cell basically consists of four types of cell.

o    α – A cell → Glucagon producing

o    β – B cell → Produce Insulin and Amylin

o    δ – D cell → Produce somatostatin


o    pp – F cell → Pancreatic polypeptide 


·         insulin is a polypeptide hormone consisting of two peptide chains that are connected by Disulphide bonds.

·         It is synthesized as a precursor (Proinsulin) that undergoes proteolytic cleavage to form insulin and C-Peptide, both of which are secreted by β-cell of the pancreas.


·         The pre-proinsulin consists of 110 amino acid residues.

·          After synthesized of 24 amino acid the pre-proinsulin is converted to proinsulin which is contain 86 amino acid residues.


·         The proinsulin cleavage to form insulin and C-peptide that contain 51 and 31 amino acid respectively.


·         The β-cells have a glucose sensing mechanism dependent on entry of glucose into β-cells (through GLUT-2) and its phosphorylation by glucokinase.

·         Glucose entry and metabolism leads to activation of the glucosensor which indirectly inhibits the ATP sensitive K+ channel (K+ ATP) resulting partial depolarization of the β-cells.

·         Increase intracellular Ca2+ availability.

·         Exocytosis release of Insulin storing granules.


·         The insulin receptor is a receptor tyrosine kinase (RTK)

·         Consisting of 2α (extracellular) and 2 intracellular β sub-units linked together by Disulphide bonds.

·         Insulin bind to α subunits site, while β subunit have tyrosine protein kinase activity.

·         After binding of insulin to β subunits induce activation of tyrosine kinase of the β subunits.

·         Phosphorylation tyrosine residues of Insulin receptor substrate protein (IRS-P).

·         Phosphorylation and dephosphorylation activate the signal and results stimulation or inhibition of enzymes involved in the rapid metabolic action of insulin.

·         PI3 – kinase generate PIP3 which mediate the action on metabolic action of Insulin.


·         PIP3 and other tyrosine phosphorylated guanine exchange protein translocate GLUT4 from cytosol to plasma membrane, especially in skeletal muscle and adipose tissue.


·         It is a peptide, gets degraded in the GIT if given orally.

·         Injected insulin metabolized primary in the liver and small extend in the kidney and muscles.

·         Half of the Insulin enters the portal vein circulation.

·         During biotransformation A and B chains of the Insulin are separated and Disulphide bonds are reduced.

·         Plasm t ½ is 5-9 minutes.


·         Hypoglycemia

·         Weight gain

·         Local injection site reaction

·         Lipodystrophy (Abnormal distribution of fats)


1.       Rapid and short acting Insulin preparation

·         Regular Insulin is a short acting, soluble, crystalline, zinc Insulin.

·         Insulin lispro, Aspart, and glulisine are rapid acting Insulin.

·         Peak level of Insulin lispro are 30-90 minutes.

·         Rapid Insulin should be administered SC. 3 minutes before meal, whereas rapid acting Insulin are administered before 15 minutes.

2.       Intermediate acting

·         Neutral protamine hagedorn (NPH)

·         Administered AC. → Not i.v.

3.       Long acting

·         The iso-electric point of insulin glargine is lower than that of human Insulin, leading to formation of precipitate at the injection site that release over an extended period.

·         Slower onset of action than NPH

4.       Insulin combination

·         Human Insulin: 70% NPH Insulin + 30% regular Insulin OR 50% of each. 

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