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excess glucose
uploaded to liver to synthesize fatty acids
lipogenesis steps
acetyl CoA → citrate → leave mitochondria → convert back into acetyl CoA → acetyl CoA units bound together to form fatty acids → become triglycerides → stored in adipocytes
excess AA
liver & kidneys use glucogenic AA to make glucose
ketogenic AA converted to acetyl CoA → ketone bodies when carbs limited
overnight fast
blood glucose falls → pancreas secretes hormone glucagon → liver increase glycogenolysis → blood glucose maintained
glycogenolysis
breakdown of glycogen into glucose
when glycogen stores are depleted…
glucagon stimulates gluconeogenesis in liver
fasting beyond glycogen depletion
body break down lean body tissue → convert glucogenic AA to glucose
once enough lean tissue → nervous tissue use ketones as fuel
how does obesity lead to insulin resistance
excess adipose tissue → proteins in adipocytes signal inflammation → cells become unresponsive to insulin
type 2 diabetes
nonalcoholic fatty liver
insulin-resistant cells don’t take up glucose & fatty acids → excess lipolysis release excess fatty acids → stimulate triglyceride synthesis in liver
metabolic syndrome
liver becomes insulin resistant so ability to regulate glycogen synthesis & gluconeogenesis affected
metabolic syndrome mechanism
glucose produced in liver → bloodstream → blood glucose rises → pancreas secretes more insulin