ecstatichamster
Member
- Joined
- Nov 21, 2015
- Messages
- 10,503
A lot of what Ray talks about is how to prevent chronically elevated stress hormones, the "stress metabolism".
But at least as far as diabetes is concerned, perhaps glucagon is the criminal here?
In this study, they induce diabetes through a routine destruction of beta cells often done in these situations with lab rats, and they found that suppressing glucagon allowed the rats to tolerate glucose Even without any increase in insulin, which was impossible because their beta cells were destroyed.
Perhaps, the idea frequently supplementing with sugar may assist in controlling glucagon levels, and may actually be more important than suppressing cortisol.
Glucagon as a Critical Factor in the Pathology of Diabetes
The surprise in the data of Lee et al. (1) comes not from the improvement in glycemia caused by a lack of glucagon action, but from the complete normalization of glucose tolerance that occurred. Transition from the fasted to fed state involves a reduction in glucose production by the liver and an increase in glucose disposal by insulin sensitive tissues (skeletal muscle, liver, and adipose tissue). Studies in the human and canine have indicated that following an oral glucose load of moderate size (∼1 g/kg BW), the liver and skeletal muscle are each responsible for approximately a third of glucose disposal, with noninsulin dependant tissues accounting for the remainder (14). In nondiabetic individuals, the changes in muscle and liver glucose metabolism are thought to be chiefly mediated by insulin (14). The fact that oral glucose tolerance was normal in the STZ treated Gcgr−/− mice of Lee et al. (1), despite no rise in insulin, suggests that in a net sense glucose uptake by liver and muscle was normal. Whether both tissues took up glucose normally, or one compensated for a defect in the other, is not clear. Nevertheless, this raises the question as to what is driving glucose disposal if not insulin.
But at least as far as diabetes is concerned, perhaps glucagon is the criminal here?
In this study, they induce diabetes through a routine destruction of beta cells often done in these situations with lab rats, and they found that suppressing glucagon allowed the rats to tolerate glucose Even without any increase in insulin, which was impossible because their beta cells were destroyed.
Perhaps, the idea frequently supplementing with sugar may assist in controlling glucagon levels, and may actually be more important than suppressing cortisol.
Glucagon as a Critical Factor in the Pathology of Diabetes
The surprise in the data of Lee et al. (1) comes not from the improvement in glycemia caused by a lack of glucagon action, but from the complete normalization of glucose tolerance that occurred. Transition from the fasted to fed state involves a reduction in glucose production by the liver and an increase in glucose disposal by insulin sensitive tissues (skeletal muscle, liver, and adipose tissue). Studies in the human and canine have indicated that following an oral glucose load of moderate size (∼1 g/kg BW), the liver and skeletal muscle are each responsible for approximately a third of glucose disposal, with noninsulin dependant tissues accounting for the remainder (14). In nondiabetic individuals, the changes in muscle and liver glucose metabolism are thought to be chiefly mediated by insulin (14). The fact that oral glucose tolerance was normal in the STZ treated Gcgr−/− mice of Lee et al. (1), despite no rise in insulin, suggests that in a net sense glucose uptake by liver and muscle was normal. Whether both tissues took up glucose normally, or one compensated for a defect in the other, is not clear. Nevertheless, this raises the question as to what is driving glucose disposal if not insulin.
