Results 1 to 1 of 1

Thread: Endocrine Effects of Insulin

  1. #1
    Administrator admin's Avatar
    Join Date
    Jan 2013
    Chengdu, Sichuan, China

    Default Endocrine Effects of Insulin


    Insulin promotes glycogen synthesis and storage while inhibiting glycogen breakdown. These effects are mediated by changes in the activity of enzymes in the glycogen synthesis pathway. The liver has a maximum storage capacity of 100 to 110 g of glycogen, or approximately 440 kcal of energy.

    Insulin increase both protein and triglyceride synthesis and VLDL formation by the liver. It also inhibits gluconeogenesis and promotes glycolysis through its effects on the function and expression of key enzymes of both pathways.

    Insulin acts to reverse the catabolic events of the postabsorptive state by inhibiting hepatic glycogenolysis, ketogenesis, and gluconeogenesis.


    Insulin promotes protein synthesis in muscle by increasing amino acid transport, as well as by stimulating ribosomal protein synthesis. In addition, insulin promotes glycogen synthesis to replace glycogen stores expended by muscle activity. This is accomplished by increasing glucose transport into the muscle cell, enhancing the activity of glycogen synthase, and inhibiting the activity of glycogen phosphorylase. Approximately 500 to 600 g of glycogen are stored in the muscle tissue of a 70-kg man, but because of the lack of glucose 6-phosphatease in this issue, it cannot be used as a source of blood glucose, except for a small amount produced when the deb ranching enzyme releases unphosphorylated glucose from brach points in the glycogen polymer, and the glucose indirectly produced via the liver from lactate generated by muscle.

    Adipose Tissue

    Fat, in the form of triglyceride, is the most efficient means of storing energy. It provides 9 kcal/g of stored substrate, as opposed to the 4 kcal/g generally provided by protein or carbohydrate. In the typical 70-kg man, the energy content of adipose tissue is about 100,000 kcal.

    Insulin acts to promote triglyceride storage in adipocytes by a number of mechanisms. It induces the produce of lipoprotein lipase in adipose tissue (this is the lipoprotein lipase that is bound to endothelial cells in adipose tissue and other vascular beds), which leads to hydrolysis of triglycerides from circulating lipoproteins, thereby yielding fatty acids for uptake by adipocytes. By increasing glucose transport into fat cells, insulin increases the availability of alpha-glycerol phosphate, a substance used in the esterification of free fatty acids into triglycerides. Insulin inhibits intracellular lipolysis of stored triglyceride by inhibiting intracellular lipase (also called hormone-sensitive lipase). This reduction of fatty acid flux to the liver is a key regulatory factor in the action of insulin to lower hepatic gluconeogenesis and ketogenesis.


    Although the brain is traditionally not considered an insulin-sensitive tissue, and overall glucose utilization by the brain is not acutely regulated by insulin, key regions of the brain can respond to insulin.

    Endocrine Effects of Insulin-screen-shot-2015-09-29-at-9-00-04-pm-png
    Last edited by admin; Tue 29th September '15 at 10:11pm.
    B.S. Pharm, West China School of Pharmacy, Class of 2007, Health System Pharmacist, RPh. Hematology, Infectious Disease. Chengdu, Sichuan, China.

    Twitter: @TomHsiung
    Sina Microblog (Weibo):

Posting Permissions

  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts