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PANCREATIC HORMONES-II

Dr.Mohammed Sharique Ahmed QuadriAssistant professorAlmaarefa College

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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

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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

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Blood Glucose and the Pancreatic Hormones

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.

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COMPLEMENTARY INTERACTION OF GLUCOSE AND INSULINE

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Counteracting action of insulin & gluccagon during absorption of high protein

SomatostatinReleased 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 result1. Inhibits digetion and absorption of nutrients2. Decreased utilization of absorbed nutrients by tissues3. 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

ofDiabetes Mellitus

References

• Human physiology by Lauralee Sherwood, seventh edition

• Text book physiology by Guyton &Hall,11th edition

• Text book of physiology by Linda .s contanzo,third edition