Global control of gluconeogenesis is mediated by glucagon ( released when blood glucose is low ); it triggers phosphorylation of enzymes and regulatory proteins by Protein Kinase A (a cyclic AMP regulated kinase) resulting in inhibition of glycolysis and stimulation of gluconeogenesis. Recent studies have shown that the absence of hepatic glucose production has no major effect on the control of fasting plasma glucose concentration. Compensatory induction of gluconeogenesis occurs in the kidneys and intestine, driven by glucagon , glucocorticoids , and acidosis. 
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Alcoholic hypoglycemia is due to inhibition of gluconeogenesis by ethanol and alcoholic ketosis is due to accumulation of beta hydroxy butyrate by increased concentrations of NADH. Thus alcoholic hypoglycemia and alcoholic ketosis are the sequential events occurring one after another in alcoholism and liver can replenish its function on supply of glucose and the most salient feature of liver is that changes in liver can be seen only after chronic alcoholism associated which is also with malnutrition. Further research is required to know the mechanism in liver that helps to maintain the reduced hepatic redox state during alcoholism longer than expected.
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Stepping back, it should be obvious that carnivores such as felines and canines provide an important source of data relevant to this question. Carnivores have colons, and they are not normally in ketosis unless food is scarce. Either their colons don't need butyrate, or they are getting sufficient butyrate from some other source. As it happens, there are microbes that ferment amino acids in to short chain fatty acids (SCFAs), including butyrate. Carnivores are known to get "animal fibre" from their prey. That is, amino acids from incompletely digested animal parts reach their colons and are fermented. In particular, in cheetahs, casein, collagen, and glucosamine have been shown to result in butyrate production comparable to fructo-oligosaccharides [Dep2012] .
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