L29 Homeostasis of plasma glucose and Diabetes Mellitus

Flashcards covering key vocabulary terms related to plasma glucose homeostasis and diabetes mellitus.

3.5 to 6 mmol/L

Normal reference range for plasma glucose concentration when fasting

3.5 to 8 mmol/L

Normal reference range for plasma glucose concentration when non-fasting

Why blood glucose concentration is important

Brain cells are dependant on glucose as energy source. Needs to be tightly regulated.

Other Cells

Can use alternative substrates for ATP production when glucose levels are low

Pancreas

Composed of head, body, and tail and located in the curve of the small intestine. Secretes insulin and glucagon.

Exocrine Glands

Secrete enzymes into ducts which empty into the intestine

Pancreatic islets (Islets of Langerhan’s)

Small clusters of endocrine cells scattered amongst acini

Alpha Cells

Secrete glucagon; increase blood glucose levels

Beta Cells

Secrete insulin; reduce blood glucose levels

Insulin

Protein hormone synthesized on RER of beta cells with A, B, and C chains. C chain removed in golgi. Released when blood glucose levels rise.

Correction of hyperglycemia

Insulin fascilitates glucose uptake into cells of most body tissue (facilitated diffusion).

Insulin receptors

Binds to alpha subunits, beta subunits get phosphate groups attached from ATP, then are able to phosphorylate proteins inside cell that mediate insulin effects (insulin response substrates.

Insulin receptors pt2

GLUT4 transporters inserted into membrane of muscle and fat cells. Causes activation/inactivation of specific enzymes pathways in cells.

GLUT4

Insulin dependant glucose transporter

Glucagon

Hormone secreted by alpha cells in response to hypOglycemia (low BGL). Acts on liver via activation of receptors that utilise cAMP as 2nd messenger. Which results in activation of enzymes.

Activation of enzymes (activated by glucagon) cause…

Glycogenolysis, gluconeogenisis, promotes release of glucose from liver cells into blood, promotes breakdown of triglycerides and release of fatty acids from adipose.

Effects of insulin of skeletal muscle.

Allows take up of glucose via GLUT4. Increased glycogen synthesis (stored glucose), transport of amino acids into muscle, and protein synthesis. Inhibits protein breakdown

Insulin on Adipose (fat tissue)

Increased glucose uptake into adipose cells via GLUT4 (facilitated diffusion). Increased synthesis and storage of triacylglycerides. Inhibits breaking down of lipids.

Effects of insulin on Liver

Inhibits gluconeogenisis, supresses formation of ketones (made when liver breaks down fat). Promotes conversion of extra glucose into fatty acids, packages into VLDL as triglyceride, which goes into blood and transports to other cells. Uptake of glucose is independant from insulin, via GLUT2.

Glycogenolysis

Breakdown of glycogen to glucose

Gluconeogenesis

Production of ‘new’ glucose from non-carbohydrate sources

Type I Diabetes Mellitus

Autoimmune destruction of beta cells. Essentially NO insulin production by beta cells. Treatment is insulin (risk hypoglycemia)

Type I Diabetes Mellitus symptoms

Related to activation of SNS; anxiety, tremor, palpatations. Due to inadequate BGL for normal brain function; headache, fatigue, dizziness, confusion.

Type II Diabetes Mellitus

Reduced sensitivity to the effects of insulin. Insulin secretion is high at first to control high BGL, eventually beta cells get worn out and secrete less insulin (hyposecretion)

Type ll diabetes causes and treatments

Caused by poor diet, obesity, some medication, and damage to pancreas. Treatments; reduce weight 10-15%, SGLT2 inhibitors (cause loss of glucose via urine), GLP-1 receptor agonists (increase insulin secretion), Metformin and acarbose.

CGMs coupled to insulin pump

CGM sends BGL to device so person can adjust insulin dose accordingly. Paired with insulin pump; pump algorithm adjusts infusion rate accordingly (can use feedfoward and feedback).