biochem exam 4: fasting state postabsorptive

what happens to glycolysis during fasting state

as blood glucose levels decline there is an increased secretion of glucagon and decrease secretion of insulin. increased glucagon/insulin ratio causes rapid mobilization of hepatic glycogen stores because of PKA mediated phosphorylation of glycogen phosphorylase kinase that phosphorylates glycogen phosphorylase

what inhibits glycogenesis during fasting

phosphorylation of glycogen synthase

what happens to gluconeogenesis during fasting state

synthesis of glucose and is released into circulation. carbon skeletons for gluconeogenesis are derived from glucogenic amino acids and lactate from muscle and glycerol from adipose tissue

what is gluconeogenesis favored by

decreased availability of allosteric inhibitor fructose 2,6-biphosphate and the subsequent activation of fructose 1,6-biphosphate

carbohydrate metabolism during fasting

liver uses glycogen degradation then gluconeogenesis to maintain blood glucose levels, presence of G6P in liver allows free glucose production

fat metabolism during fasting

liver maintaining blood glucose levels, uses FA oxidation as major source of energy and synthesizes ketone bodies

what happens to increased FA oxidation during fasting

oxidation of FAs obtained from TAG hydrolysis in adipose tissue and is the major energy source in hepatic tissue.

What does FA oxidation generate during fasting

NADH, FADH2, and acetyl-CoA

What does NADH inhibit

inhibits the TCA cycle and shift OAA to malate which results in acetyl-CoA being available for ketogenesis

Increase ketogenesis during fasting

liver releases 3-hydroxybutyrate and acetoacetate for fuel by peripheral tissues. the liver itself doesn’t use ketones. It also releases CoA for FA oxidation

when does ketogenesis start

first days of fasting when acetyl-CoA from FA oxidation exceeds the oxidative capacity of the TCA cycle

what happens to adipose tissue in fasting state

• carbohydrate metabolism- glucose transport by GLUT-4 into adipocyte and its subsequent metabolism is decreased and results in decreased TAG synthesis

• fat metabolism- adipose is second to distribute energy compounds to rest of body. cells hydrolyze stored TAGs providing free FAs in blood and tissue

• increased fat degradation- PKA-mediated phosphorylation and activation of HSL and subsequent hydrolysis of TAGs are enhanced by elevated norepinephrine and epinephrine

• increased FA release

• decreased FA uptake- LPL activity of adipose tissue is low, FAs from circulating TAGs in lipoprotein complexes are less available

resting skeletal muscle in fasting state

• carbohydrate metabolism- glucose transport into skeletal myocyte, subsequent glucose metabolism is decreased by low insulin levels, glucose from hepatic gluconeogenesis is unavailable

• lipid metabolism- muscle tissue uses FAs from adipose and ketone bodies. muscle decrease use of ketone bodies during prolonged fasting and oxidizes FAs. epinephrine signals increase LPL expression and uptake more FA

• protein metabolism- rapid breakdown of muscle protein

brain in fasting state

brain only uses glucose for fuel, blood glucose is maintained by hepatic gluconeogenesis, in prolonged fasting plasma ketone bodies replace glucose for brain fuel and reduced protein catabolism for gluconeogenesis

absorptive state: intestines lead to

increase of glucose, amino acids, and fatty acids in the intestine

absorptive state: what does increase of glucose, AAs and fatty acids in intestine and portal lead to

increase of glucose and AA in portal veins

Absorptive state: increase of glucose and AAs in portal vein leads to

increase in insulin release by beta cells of the pancreas and decrease in release of glucagon by alpha cells of the pancreas

absorptive state 1: increased insulin release and decrease glucagon release in pancreas leads to

increase in lipoprotein lipase levels, synthesis of triacylglycerols, and uptake of glucose and fatty acids in adipose tissue

absorptive state 2: increased insulin release and decrease glucagon release in pancreas leads to

increased synthesis of glycogen, fatty acids, triacylglycerols, and synthesis of VDLs in the liver

absorptive state 3: increased insulin release and decrease glucagon release in pancreas leads to

increased uptake of glucose, synthesis of glucagon, and synthesis of protein in muscles

absorptive state 4: increased insulin release and decrease glucagon release in pancreas leads to

glucose completely oxidized to carbon dioxide and water in the brain

what does absorptive state help provide

capture of energy as glycogen and triacylglycerols and replenishment of any protein degraded during previous postabsorptive period

fasting state: in the intestines and portal veins

nutrients in the intestine lease to decrease in amino acids and glucose in blood

fasting state: decrease in AAs and glucose in blood leads to

decrease in release of insulin by beta cells and increase in release of glucagon by alpha cells in the pancreas

fasting state 1: decrease in insulin release and increase in glucagon release leads to

increase of released FAs produced by hydrolysis of triacylglycerol in adipose tissue

fasting state 1: decrease in insulin release and increase in glucagon release leads to

increased release of glucose produced by glycogen degradation, release of glucose produced by gluconeogenesis, and release of ketone bodies in the liver

fasting state 2: decrease in insulin release and increase in glucagon release leads to

increased lipoprotein lipase levels, use of FAs and ketone bodies, and release of amino acids in muscles

fasting state 3: decrease in insulin release and increase in glucagon release leads to

glucose and ketones completely oxidized to carbon dioxide and water

the release of glucose and ketone bodies in the liver provides for

glucose for brain and other glucose-requiring tissues

release of FAs in adipose tissue provides for

FA and ketones as fuels for non-glucose-requiring tissues