Alterations of Glucose-Dependent Insulinotropic Polypeptide and Expression of Genes Involved in Mammary Gland and Adipose Tissue Lipid Metabolism during Pregnancy and Lactation
Figure 9
Simplified schematic depicting possible role of GIP-R and other key regulators in mammary and adipose tissue metabolism.
It is envisaged that GIP increases uptake of free fatty acids and glucose by stimulating LPL and GLUT4 expression, favouring triglyceride formation. There is evidence that GIP also inhibits HSD-1 which, by limiting local cortisol production, restrains HSL and lipolysis. Other key actions on lipolysis via HSL are mediated by GCG-R, ESS-RA, Prl-R and adrenergic receptors [17], [30], [31]. α2A-AdR, α2 adrenergic receptor; acetyl CoA carboxylase-1, ACC-1; fatty-acid transport protein, Fat-P; glucagon receptor, GCG-R; GIP receptor, GIP-R; glucose transporter type 4, GLUT4; 11β-hydroxysteroid dehydrogenase type 1, HSD-1; hormone-sensitive lipase, HSL; lipoprotein lipase, LPL; oestrogen receptor A, ESS-RA; oestrogen receptor B, ESS-RB and prolactin receptor, Prl-R.