Glucagon Ketosis

Hypoglycemia lack of glycogenolysis by epinephrine or glucagon ketosis, hyperlipidemia, hyperuricemia hepatomegaly autosomal recessive. Galactose and fructose not converted to glucose. 

Diazoxide is a potassium channel opener with a rapid antihypertensive action after intravenous administration. Diazoxide causes hyperglycaemia which may underlie side-effects such as nausea and vomiting, cardiac dysrhythmia and ketosis. Diazoxide was used occasionally in the management of hypertensive emergencies, but it is now largely abandoned for this indication. Diazoxide is an alternative for glucagons in patients with hypogycaemia. 

Because insulin normally inhibits lipolysis, a diabetic has an extensive lipolytic activity in the adipose tissue. As is seen in Table 21.4, plasma fatty acid concentrations become remarkably high. /3-Oxidation activity in the liver increases because of a low insulin/glucagon ratio, acetyl-CoA carboxylase is relatively inactive and acyl-CoA-camitine acyltransferase is derepressed. /3-Oxidation produces acetyl-CoA which in turn generates ketone bodies. Ketosis is perhaps the most prominent feature of diabetes mellitus. Table 21.5 compares ketone body production and utilization in fasting and in diabetic individuals. It may be seen that, whereas in the fasting state ketone body production is roughly equal to excretion plus utilization, in diabetes this is not so. Ketone bodies therefore accumulate in diabetic blood. 

Only in the 1960 s was it established that peripheral tissue, such as heart and kidney, could actively metabolize ketone bodies to use as respiratory fuel. In fact, glucose and fatty acids complement each other as respiratory fuels. Consequently, when glucose is low (starvation or ketosis in cattle) or unavailable (diabetes), glucagon is secreted, inducing lipogenesis in adipose tissue with liberation of free fatty acids. 

The oxidation rate of fatty acids appears to be proportional to the concentration in plasma, and, as mentioned above, major products are ketone bodies, which can serve as respiratory fuel. In moderate forms of ketosis, glucagon secretion is antagonized by that of insulin consequently ketone bodies do not accumulate because g their utilization by peripheral tissues is accelerated and their genesis interrupted. In several forms of ketosis, homeostasis breaks down. In diabetics, the lipolytic effect of glucagon is not compensated for, and the increase in free fatty acids and ketone bodies in plasma is unchecked. Moreover, utilization of ketone bodies by peripheral tissue could be reduced. 

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