Question

In which hormone scenario are fatty acids synthesized or anabolized from other macronutrient sources? +insulin +glucagon +epenephrine

Answer 1

ANSWER INSULIN LEAD TO SYNTHESIS OF FATTY ACID WHILE GLUCAGON AND EPINEPHRINE ARE INVOLVED IN DEGRADATION OF LIPIDS AND BETA OXIDATION

EXPLANATION

High plasma levels of insulin in the blood plasma (e.g. after meals) cause the dephosphorylation of acetyl-CoA carboxylase, thus promoting the formation of malonyl-CoA from acetyl-CoA, and consequently the conversion of carbohydrates into fatty acids.Insulin stimulates fatty acid synthesis in white and brown fat cells as well as in liver and mammary tissue.

Epinephrine and glucagon (released into the blood during starvation and exercise) cause the phosphorylation of enzyme, inhibiting lipogenesis in favor of fatty acid oxidation via beta-oxidation.Glucagon ensures energy supply by mobilizing lipids. In the fasting state, glucagon is secreted and insulin concentrations are not sufficient to inhibit lipolysis in adipocytes, where lipids are stored in lipid droplets consisting of a core of triglycerols (TG) and sterols esters coated with perilipins (P) (proteins restricting access to the lipid core). In response to an appropriate stimuli, e.g., epinephrine along with glucagon, ADENYLATE CYCLASE (AC) found in the plasma membrane of the adipocyte is activated, leading to increased intracellular concentrations of cAMP stimulating protein kinase A (PKA) activity. PKA phosphorylates (hence activates) hormone sensitive lipase (HSL) and P. The phosphorylation of P results in dissociation of the protein CGI-58. CGI-58 activates adipose triglycerol lipase (ATGL), which converts TGs to diaglycerols (DG). The phosphorylated P bind HSL and allows it to access the lipid droplet where it coverts DGs to monoglycerols (MG). The monoglycerols are hydrolyzed by monoacylglycerol lipase (MGL), yielding free fatty acids (FFAs) and glycerol, which are released to the blood. FFAs may stimulate glucagon secretion, and glucagon in turn stimulates hepatic gluconeogenesis , glycogenolysis, and beta-oxidation thus providing substrates for the liver to secure sufficient energy supply to metabolically active tissue.