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Comment
. 2011 Feb;60(2):377-80.
doi: 10.2337/db10-1594.

Glucagon as a critical factor in the pathology of diabetes

Dale S Edgerton  1 , Alan D Cherrington
Affiliations
Comment

Glucagon as a critical factor in the pathology of diabetes

Dale S Edgerton et al. Diabetes. 2011 Feb.
No abstract available

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Figures

FIG. 1.
FIG. 1.
A: In the normal state, a meal-related rise in circulating glucose is efficiently cleared as the result of reciprocal changes in plasma insulin and glucagon concentrations. Increased glucose disposal is primarily accounted for by liver and skeletal muscle. Insulin increases disposal by both organs whereas glucagon opposes insulin at the liver. Insulin also inhibits lipolysis, thus reducing circulating NEFA and further promoting HGU and MGU. It is unclear what role glucagon may play in regulating lipolysis, although it appears to be minor. B: In type 1 diabetes, insulin is lacking and the effects of glucagon are unopposed. Glucose disposal is reduced as a result of the inhibitory effects of glucagon on the HGU and lack of insulin stimulated HGU and MGU. Plasma NEFAs are elevated, perhaps in part as a result of glucagon mediated stimulation of adipose tissue lipolysis in the absence of insulin. Reduced glucose clearance and increased glucose production leads to glucotoxicity, which in combination with lipotoxicity, further impairs glucose clearance. C: In STZ-treated Gcgr−/− mice, fasting NEFA levels are low, possibly because of the lack of glucagon action. GLP-1 levels are increased, and together with low NEFA, may create an adaptive state in which glucose disposal occurs normally in the absence of insulin and glucagon signaling. (A high-quality color representation of this figure is available in the online issue.)
See this image and copyright information in PMC

Comment on

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