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ILO’S 
1. Introduction 
2. Synthesis & Metabolism 
3. Insulin secretion 
4. Physiological roles 
5. Insulin effects 
6. Deficiency of insulin 
7. Symptoms 
8. Excess of Insulin 
9. Oral Hypoglycaemic Agents 
10.Synthesis
It was first isolated in 1921 by Banting and Best and therapeutically 
used in 1922. 
Human insulin now been produced from E-coli by recombinant DNA 
technology.
(1) Proinsulin is the immediate precursor to insulin in the single-chain 
peptide. 
(2) Proinsulin folds to adopt the ‘correct orientation of the prevailing 
‘disulphide bonds’ plus other relevant conformational constraints 
whatsoever on account of its primary structure exclusively. 
(3) Proinsulin in reality, has a precursor of its own, preproinsulin–a 
peptide, that essentially comprises of hundreds of ‘additional residues’. 
(4) At an emerging critical situation the insulin gets generated from 
proinsulin due to the ensuing cleavage of proinsulin at the two points 
indicated. 
This eventually produces insulin.
Normal blood 
glucose level: 
70-90 mg/100ml
CLASSIFICATION OF ORAL HYPOGLYCEMIC AGENTS 
(i)Sulfonylureas: 
First-Generation Sulfonylureas: Acetohexamide ; Chlorpropamide ; Tolazamide 
Second-Generation Sulfonylureas: Glipizide ; Glyburide ; Glumepiride 
(ii) Non sulfonylureas: repaglinide, nateglinide 
(iii) Thiazolindiones: Rosiglitazone, Troglitazone 
(iv) Bisguanides: metoformin, phenoformin 
(v) α-Glucosidase Inhibitors: Acarbose
Sulfonylureas 
SAR : 
(1) These are urea derivatives having an arylsulfonyl moiety in the 1 position and an 
aliphatic function at the 3-position. 
(2) The aliphatic moiety, R′, essentially confers lipophilic characteristic properties to the 
newer drug molecule. 
(3) Optimal therapeutic activity often results when R′ comprises of 3 to 6 carbon atoms, as 
in acetohexamide, chlorpropamide and tolbutamide. 
(4) Aryl functional moieties at R′ invariably give rise to toxic compounds. 
(5) The R moiety strategically positioned on the ‘aromatic ring’ is primarily responsible for 
the duration of action of the compound.
Insulin  rohit bharti
Insulin  rohit bharti
Insulin  rohit bharti
Insulin  rohit bharti
Insulin  rohit bharti

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Insulin rohit bharti

  • 1.
  • 2. ILO’S 1. Introduction 2. Synthesis & Metabolism 3. Insulin secretion 4. Physiological roles 5. Insulin effects 6. Deficiency of insulin 7. Symptoms 8. Excess of Insulin 9. Oral Hypoglycaemic Agents 10.Synthesis
  • 3. It was first isolated in 1921 by Banting and Best and therapeutically used in 1922. Human insulin now been produced from E-coli by recombinant DNA technology.
  • 4.
  • 5.
  • 6. (1) Proinsulin is the immediate precursor to insulin in the single-chain peptide. (2) Proinsulin folds to adopt the ‘correct orientation of the prevailing ‘disulphide bonds’ plus other relevant conformational constraints whatsoever on account of its primary structure exclusively. (3) Proinsulin in reality, has a precursor of its own, preproinsulin–a peptide, that essentially comprises of hundreds of ‘additional residues’. (4) At an emerging critical situation the insulin gets generated from proinsulin due to the ensuing cleavage of proinsulin at the two points indicated. This eventually produces insulin.
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  • 10.
  • 11.
  • 12.
  • 13.
  • 14.
  • 15. Normal blood glucose level: 70-90 mg/100ml
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  • 19.
  • 20. CLASSIFICATION OF ORAL HYPOGLYCEMIC AGENTS (i)Sulfonylureas: First-Generation Sulfonylureas: Acetohexamide ; Chlorpropamide ; Tolazamide Second-Generation Sulfonylureas: Glipizide ; Glyburide ; Glumepiride (ii) Non sulfonylureas: repaglinide, nateglinide (iii) Thiazolindiones: Rosiglitazone, Troglitazone (iv) Bisguanides: metoformin, phenoformin (v) α-Glucosidase Inhibitors: Acarbose
  • 21. Sulfonylureas SAR : (1) These are urea derivatives having an arylsulfonyl moiety in the 1 position and an aliphatic function at the 3-position. (2) The aliphatic moiety, R′, essentially confers lipophilic characteristic properties to the newer drug molecule. (3) Optimal therapeutic activity often results when R′ comprises of 3 to 6 carbon atoms, as in acetohexamide, chlorpropamide and tolbutamide. (4) Aryl functional moieties at R′ invariably give rise to toxic compounds. (5) The R moiety strategically positioned on the ‘aromatic ring’ is primarily responsible for the duration of action of the compound.