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. Author manuscript; available in PMC: 2017 May 10.
Published in final edited form as: Cell Metab. 2016 May 10;23(5):770–784. doi: 10.1016/j.cmet.2016.04.011

Figure 3. A working model of adipocyte/islet communication.

Figure 3

Leptin inhibits insulin and glucagon secretion from β- and α-cells, respectively. Whether this is a direct action of leptin or centrally mediated has not been entirely elucidated. The effects of adiponectin on β -cell insulin secretion may depend on circulating glucose concentration, with adiponectin inhibiting insulin secretion at low glucose concentrations and stimulating insulin secretion at high glucose concentrations. Fatty acids enhance glucose stimulated insulin secretion at high glucose conditions. Under fasting conditions, fatty acids may increase glucagon secretion indirectly by limiting somatostatin’s inhibitory effect on α-cell exocytosis and fasting-induced decreases in leptin secretion may act to relieve leptin’s inhibitory effect on glucagon secretion under low blood glucose concentrations.