Insulin Hormone Sensitive Lipase Ketoacidosis

\ FFA release

f Glycogen, glucose uptake Liver

Brain

> Adipose tissue J HSL, ATGL

I HGP ▲Jglycogenolysis, I [gluconeogenesis

GlucagonV

FFAs

LPL-mediated lipolysis

Insulin

Skeletal muscle

Pancreas

Insulin action

Brain

> Adipose tissue J HSL, ATGL

Insulin Tissue

Adipose tissue

Insulin action

Skeletal muscle t Glucose uptake Î FA esterification I TG lipolysis

Adipose tissue

Insulin action

Skeletal muscle

Glucose uptake t Glucose uptake Î FA esterification I TG lipolysis

Fig. 1. Glucose and FFA homeostasis. A. Postabsorptive/fasting period: Stimulation of adipose tissue lipases, HSL and ATGL, by low plasma insulin concentrations and elevated glucagon, facilitates mobilization of stored triglycerides, releasing fatty acids into the circulation. Low insulin and high glucagon also stimulates gluconeogenesis from FFA and other gluconeogenic substrates and facilitates fatty acid transport into the mitochondria of hepatocytes, where they are utilized for ^-oxidation and formation of ketone bodies. B. Postprandial period: Insulin is secreted by pancreatic ^-cells in response to rising blood glucose, FFA and other secretatogogues. Insulin inhibits hepatic glucose production and stimulates glucose uptake, utilization and storage in insulin sensitive tissues such as muscle, liver and adipose tissue. Adipose tissue lipolysis is suppressed and lipolysis of triglyceride rich lipoproteins (chylomicrons and VLDL) by lipoprotein lipase is stimulated by insulin, with net fatty acid uptake by adipose tissue. Hepatic glucose production is suppressed and glycogen storage stimulated by direct insulin action as well as indirectly by suppression of plasma FFAs and by neuronal signals eminating from the hypothalamus, which senses nutrients directly. Abbreviations are: ATGL = adipose triglyceride lipase; FA = fatty acid; FFAs = free fatty acids; HGP = hepatic glucose production; HSL = hormone sensitive lipase; LPL = lipoprotein lipase; VLDL = very low density lipoprotein (see Color Plate 2, following p. 34).

nutrient-induced insulin secretion. The postprandial rise of plasma glucose, fatty acids, amino acids, and incretin hormones stimulates the release of insulin by pancreatic ^-cells, which serves to stimulate glucose uptake by insulin sensitive tissues such as muscle and adipose tissue and suppresses glucose production by liver and kidney (Fig. 1 and Color Plate 2, following p. 34). In addition, insulin suppresses FFA release from adipose tissue and favors their storage as TGs. Maintenance of whole-body glucose and lipid homeostasis depends upon normal insulin secretion by pancreatic ^-cell and normal tissue sensitivity to insulin (1,2).

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