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Diabetes Mellitus

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Physiology 3120
Tom Stavraky

Human Physiology Monday, March 1, 2010 “Endocrine V” Diabetes Mellitus • Diabetes – Greek (large volume of urine); mellitus – Latin (a sweet taste)  Once tested for by observing whether ants would swarm around a person’s urine; therefore referred to as “sweet urine disease” (Madhumeha) • Characterized by hyperglycemia (too much glucose in bloodstream); polyphagia (eating frequently); polyuria; glycosuria (glucose in the urine); water and electrolyte loss • In severe cases, get ketosis (build-up of ketones in bloodstream), acidosis, coma and death • Long-term complications: retinopathy (damage to retina or lens; get expansion and contraction); nephropathy; angiopathy • Insulin stimulates. . .  Glucose uptake  • Diabetes mellitus  Type I  Insulin-dependent; failure to secrete sufficient insulin to regulate glucose utilization  Autoimmune destruction of pancreatic B-islet cells; B-islet cells produces proteins after an “insult” that promote immune reaction; the cascade is fairly rapid once it’s initiated  Early onset  Only ~10% of diabetics  Inability to import glucose; alternate energy source needed • Protein o Increased gluconeogenesis (mostly in liver) o Muscle broken down to AA, which is converted into glucose in liver; causes (I) muscle wasting and (II) weight loss • Fat (more predominant) o Increased lipolysis o Mobilization of triglycerides and free fatty acids (FFAs) for energy; clipped into acetyl-CoA, which can then enter the citric acid cycle o By-products are ketones (results in ketosis)  Fate of high serum glucose • Increased glucose filtration = water excretion = dehydration • Glucose converted to sorbitol (via the “polyol pathway”) which damages the lens, nerves, and capillaries • Increased glycosylation of proteins (via the “glyoxal pathway”; especially haemoglobin); end-products are diagnostic (levels of glycosylated haemoglobin resides in serum for a long time) and damaging  Type II  Insulin resistant/impaired insulin secretion; overall, a decreased cellular response to insulin  “Lifestyle” – overweight and sedentary  Onset in mid-life (now seeing more and more cases in juveniles)  ~90% of diabetics  Complex interplay of factors contribute to insulin resistance • Lifestyle o Muscle is major user of glucose, so regular exercise maintains the tuning of the insulin release system • Diet o Tend to eat high-fat and high-salt foods (maybe an evolutionary drive) • Genes  Leads to obesity and insulin resistance (most obese people are also IR); also leads to PCOS; increases visceral fat (behaves differ
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