Control of Blood Glucose and Diabetes Management

Glycogenesis

Conversion of glucose to glycogen in liver.

Glycogenolysis

Breakdown of glycogen to glucose.

Gluconeogenesis

Production of glucose from non-carbohydrates.

Lipolysis

Breakdown of stored fat into fatty acids.

Gestational Diabetes

Diabetes occurring during pregnancy, resolves postpartum.

Microangiopathy

Thickening of small blood vessel walls.

Retinopathy

Diabetes-related blindness risk increased 25 times.

Nephropathy

Diabetes-related renal failure risk increased 17 times.

Neuropathy

Nerve damage causing postural hypotension, impotence (erectile dysfunction), foot ulcers.

Why is glucose homeostasis important

CNS relies entierly on glucose as its energy source, unlike muscles, which can utilise fat, brain cannot due to the blood-brain-barrier

Name the prime glucose homeostasis regulators and describe their function

insulin-secreted when glucose levels are high, it reduces blood glucose levels and promotes its storage and use

glucagon-secreted when glucose levels are low, it increases blood glucose and promotes its breakdown from glycogen

adrenaline- increases blood glucose during stress/fear

cortisol- prolonger high cortisol induces diabetes like symptoms

growth hormone-high GH leads to hyperglycemia

Describe insulin secretion

glucose enters the pancreatic beta cells via glucose transporters, where it's metabolised to ATP, which causes K channels to close and Ca channels to open, Ca influx triggers the release of insulin via secretory vesicles, that contain pro-insulin, the enzyme that chops of C-peptide and Zn for insulin crystals

Describe factors which stimulate insulin secretion

increased blood glucose, amino acids, secretin gut hormone, glucagon, adrenaline

Describe the fed and fasting state in the liver

fed state-glycogenesis, fat synthesis

fasting state-glycogenolysis, gluconeogenesis

Describe the fed and fasting state in the muscle

fed state-glycogen storage, muscle synthesis

fasting state- protein breakdown, fatty acid use

Describe the fed and fasting state in the adipose tissue

fed state-fat storage

fasting state- lipolysis, fatty acid release

Describe what happens in the brain and red blood cells

no insulin or glucagon effect, only glucose dependant

Describe the procedure for glucose tolerance test

baseline measurement after overnight fasting, then 75 mg of glucose is consumed, and blood glucose is measured every 30min, 1h and 2h

Describe the glucose tolerance curve for normal, type 1 and type 2 diabetes

normal-blood glucose peaks within 30min to 1h and goes back to baseline within 2h

type 2- higher fasting glucose, prolonged glucose peak, which exceeds the renal threshold, with delayed return to baseline

type 1- fasting glucose starts higher and rise sharply after glucose digestion and remain elevated

Briefly describe type 1 diabetes

autoimmune destruction of beta cells, symptoms include hyperglycaemia, polyuria, polydipsia, polyphagia, muscle wasting, weight loss and ketoacidosis

treatment is insulin

Briefly describe type 2 diabetes

insulin resistance or reduced insulin sensitivity, symptoms are milder than type 1 and ketoacidosis is rare

treatment includes weight loss, lifestyle changes, oral hypoglycaemic agents and in advanced cases insulin

Describe the chronic complications of diabetes

microangiopathy, retinopathy, nephropathy, neuropathy

ketoacidoisis

medical emergency due to excessive fat breakdown leading to the production of acidic ketone bodies causing low pH

polyuria

excessive urination

polydipsia

increased thirst

polyphagia

hunger