PANCREATIC HORMONES-II Dr.Mohammed Sharique Ahmed Quadri Assistant professor Almaarefa College 1

Objectives Describe the regulation of pancreatic hormone secretions Illustrate the mechanisms of action of glucagon Discuss the physiological effects glucagon Discuss the pathophysiology of Diabetes mellitus 2

Pancreatic Hormones Glucagon – Mobilizes energy-rich molecules from storage sites during postabsorptive state – Secreted in response to a direct effect of a fall in blood glucose on pancreatic α cells – Generally opposes actions of insulin Glucagon is the hormone of "starvation." - It produces hyperglycemia 3

Blood Glucose and the Pancreatic Hormones 4

Actions of Glucagon ON CARBOHYDRATE:  Stimulates hepatic glycogenolysis.  Increases gluconeogenesis. ON FAT:  Promotes fat breakdown and inhibits triglyceride syntheis -  FFA and glycerol in blood -used for gluconeogenesis - Oxidation for energy (Ketogenesis) ON PROTEIN:  Inhibits protein synthesis - Proteolytic Effects Glycogenolytic, Gluconeogenic, Lipolytic, Ketogenic Hormone.

COMPLEMENTARY INTERACTION OF GLUCOSE AND INSULINE 6

Counteracting action of insulin & gluccagon during absorption of high protein 7

Somatostatin Released from pancreatic D cells in direct response to increase in blood sugar and blood amino acids during absorption of a meal Inhibitory effect on both insulin and glucagon Decreases motility of stomach, duodenum and gallbladder Decreases secretion and absorption in the gastrointestinal tract End result 1.Inhibits digetion and absorption of nutrients 2.Decreased utilization of absorbed nutrients by tissues 3.Extends the availability of nutrients for longer periods of time

Diabetes Mellitus Most common of all endocrine disorders Prominent feature is elevated blood glucose levels – Urine acquires sweetness from excess blood glucose that spills into urine Two major types – Type I diabetes Characterized by lack of insulin secretion – Type II diabetes Characterized by normal or even increased insulin secretion but reduced sensitivity of insulin’s target cells

Type I Diabetes Mellitus (juvenile onset /IDDM) 10 % of D.M Cases No / nearly no insulin Autoimmune process- selective destruction of β- cells Precise cause unknown – Genetic susceptibility – Environmental triggers Treatment : Insulin Dietary control Exercise

Type II Diabetes Mellitus (Maturity onset /NIDDM) 90 % of D.M Cases Normal / increase insulin secretion Decrease sensitivity of target cells to insulin i.e. insulin resistance Cause : – Ultimate cause unknown – Various Genetic & lifestyle factors – Obesity is biggest risk factor ( 90% are obese)

Type II Diabetes Mellitus (Maturity onset /NIDDM) – Link between obesity and insulin resistance Adipokines secreted by adipose tissue modulate response of target tissue o insulin – Resistine( promotes resistance ), increases in obesity – adiponektin (increase insulin sensitivity), decreases in obesity Increase FA can indirectly triggers the apoptosis ofβ-cells Treatment : Dietary control Exercise Oral hypoglycemic agents

Acute Effects of Diabetes Mellitus

References Human physiology by Lauralee Sherwood, seventh edition Text book physiology by Guyton &Hall,11 th edition Text book of physiology by Linda.s contanzo,third edition