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37 Cards in this Set
- Front
- Back
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hormones that have both catabolic and anabolic effects
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growth hormone
thyroxine |
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glucagon and GH
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both increase blood glucose levels
the hyperglycemia induced by glucagon eventually inhibits growth hormone release initially GH release is stimulated by glucagon to ensure maximum increase in blood glucose both also increase lipolysis and ketogenesis |
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paradoxical effect of GH
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GH increases plasma glucose but also stimulates insulin release from cells and promotes glycogen storage in the liver
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cortisol paradoxical effect
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increases blood glucose while also promoting glycogen storage in the liver
does this as the body needs glucose to respond to stress and then stores it in the liver to sequester the response |
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absorptive state
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carbs most important energy source
synthesis of carbs, triglycerides, and proteins liver takes up glucose and stores as glycogen AAs --> proteins |
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postabsorptive state
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maintain blood glucose
breakdown of glycogen, triglycerides, and protein brain uses mostly glucose but increases use of ketones if fasting persists |
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effects of insulin
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actions in muscle, fat, and liver
increases glucose uptake and use in cells increases synthesis of proteins, fats, and carbs |
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effects of glucagon
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actions mainly in muscle and fat
increases blood glucose |
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Amino Acid effects on glucagon and insulin levels
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increased AA --> increased glucagon and insulin
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glucagon and insulin levels after a mixed protein-carb meal
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both are increased
insulin is increased more than glucagon as both carbs and AAs lead to increases in insulin and only AAs lead to increase in glucagon |
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insulin-glucagon interaction
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in pancreas: insulin inhibits alpha cells limiting glucagon release
In liver: insulin only affects previously glucagon activated cells |
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epi effects on blood glucose
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increase blood glucose by:
glycogenolysis gluconeogeneis lipolysis inhibiting insulin release stimulating glucagon release |
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sympathetic nerve stimulation of liver and adipose tissue
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same effects as epi
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effect of increased cortisol levels
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increased blood glucose, AAs, and FAs
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prolonged high levels of cortisol can cause symptoms similar to
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insulin deficiency
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life-threatening hypoglycemia can result in this type of patient
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cortisol deficient
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high levels of growth hormone
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increase blood glucose
mobilizes lipids |
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GH, IGF-1, and insulin response to protein ingestion
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GH: increased
IGF-1: increased Insulin: increased |
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GH, IGF-1, and insulin response to carb ingestion
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GH: decreased
IGF-1: none Insulin: increased |
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GH, IGF-1, and insulin response to fasting
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GH: increased
IGF-1: decreased Insulin: decreased |
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Exercise
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muscles use:
glycogen from muscles producing lactate/pyruvate glucose from liver FAs from adipose tissue lipolysis |
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ghrelin
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produced in stomach
increases appetite short-term (1-2 hrs. before meal) |
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CCK
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produced by I cells of duodenum and jejunum
decreases appetite short-term (after food leaves stomach) |
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PYY3-36
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produced in SI
decreases appetite between meals |
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leptin
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produced in white adipose tissue
decreases appetite via decreased neuropeptide Y long-term ongoing regulation |
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Orexin
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produced in lateral hypothalamus
increases appetite ongoing reg |
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type 1 DM
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low or no insulin due to autoimmune destruction of beta cells
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consequences of type 1 DM
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always elevated blood glucose
marked lipolysis --> elevated glycerol and FAs elevated ketones as liver converts FAs to ketones |
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untreated type 1 DM
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elevated glucose and ketones causes osmotic diuresis --> decreased blood volume --> decreased brain blood flow --> coma
elevated ketones --> increased plasma H+ --> acidosis --> brain dysfunction --> coma |
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obesity and type 2 DM
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greater levels of insulin are required to control blood glucose in obese patients
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glucagon and DM severity
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glucagon is elevated or normal in many DM patients even though blood glucose is high as direct suppression of glucagon release by insulin is suppressed
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conditions resulting in very low blood glucose
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insulin-producing tumors
excess insulin injection liver disease glucagon def. cortisol def. |
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symptoms of hypoglycemia
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due to low plasma glucose: headache, confusion, poor coordination
due to reflexive sympathetic action: hunger, tachycardia, tremors, weakness, anxiety |
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food intake and fat oxidation
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inhibits fat oxidation
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diet and exercise plan with greatest potential to yield a long-term, slow-rate negative fat balance
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medium carb, low-fat diet
prolonged low-moderate intensity exercise |
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BMI
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body weight/height^2
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BMI > 30
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obese
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