Ketosis Diabetes

C7. Chen, J. C., Marster.s, E,., and Wieland, E. G., Diabetic ketosis. Interpretation of elevated serum glutamic-oxaloacetic transaminase (SCOT) by multichannel chemical analysis. Diabetes 19, 730-731 (1970). 

In moderate metabolic acidosis which occurs in cases of mild renal insufficiency, infant diarrhoea, diabetic ketosis etc. 

Direct Test on Urine Glucose, ketones, and pH— Labstix test Dip a Labstix strip briefly into the urine and read after 10 to 15 seconds. For glucose, the result should be correlated with blood-glucose determination. A positive result for ketones may indicate intoxication by acetone or isopropyl alcohol. This test may also be positive in starvation or in diabetic ketosis. 

Ketones commonly are elevated in the blood in states of starvation, as the body calls upon its fatty acids (stored as triglycerides) to break down and provide fuel. Ketones may also be elevated in diabetes mellicus, where glucose does not enter the cell and carmot be efficiently utilized. Triglycerides then break down to provide the fetty acids and acetyl CoA useful as fuel, sometimes with formation of ketones as well. In severe diabetic ketosis, one may actually detect the smell of acetone coming from the patient. 

Certain pathological conditions can lead to a life-threatening rise in the blood levels of the ketone bodies. Most common of these conditions is diabetic ketosis in patients with insulin-dependent diabetes mellitus. The absence of insulin has two major biochemical consequences. First, the liver cannot absorb glucose and consequently cannot provide oxaloacetate to process fatty acid-derived acetyl CoA (Section 17.3.1). Second, insulin normally curtails fatty acid mobilization by adipose tissue. The liver thus produces large amounts of ketone bodies, which are moderately strong acids. The result is severe acidosis. The decrease in pH impairs tissue function, most importantly in the central nervous system. 

It is usually easier to differentiate hypoglycaemia from severe diabetic ketosis than from other causes of coma, which are as likely in a diabetic as in anyone else. It is unsound to advocate blind administration of i.v. glucose to comatose diabetics on the basis that it will revive them if they are hypoglycaemic and do no harm if they are hyper-glycaemic. A minority of comatose insulin-dependent diabetics have hyperkalaemia and added glucose can cause a brisk and potentially hazardous rise in serum potassium (mechanism uncertain), in contrast to nondiabetics in whom glucose causes a fall in serum potassium. 

Mild diabetic ketosis. If the patient is fully conscious and there has been no nausea or vomiting for at least 12 h, intravenous therapy is unnecessary. It is reasonable to give small doses of insulin s.c. 4-6-hourly and fluids by mouth. 

When a surgical emergency is complicated by diabetic ketosis, an attempt should be made to control the ketosis before the operation. Management during the operation will be similar to that for major surgery except that more insulin will be needed. 

Fery, F., and Balasse, E. O. (1985). Ketone body production and disposal in diabetic ketosis. Diiiiwles 34, 326-332. 

Figure 22.23 Diabetic ketosis results when insulin is absent. In the absence of insulin, fats are released from adipo.se Tissue, and glucose cannot be absorbed by the liver or adipose tissue. The liver degrades the fatty acids by p oxidation but cannot process the acetyl CoA, because of a lack of glucose-derived oxaloacetate (OAA).

Hypersensitivity, urticaria, anaphylactic shock Acute hemorrhagic pancreatitis pancreatitis, with decreased serum insulin diabetic ketosis... 

Two types of subunits are distinguishable M (muscle) type and H (heart) type- Lactate dehydrogenases of heart and muscle are mainly H4 and M4 all other possible hybrids have been found in various tissues. Elevations of lactate dehydrogenase activity have been found in myocardial infarction, hepatocellular necrosis, metastatic carcinoma, diabetic ketosis, sickle cell anemia, malignant lymphoma, infectious mononucleosis, and cerebral infarction Standjord el of., J. Am. Med. Assoc. 182, 1099 (1962). Comprehensive reviews Everse, Kaplan, Ad van. Enzymol. Helot. Areas Mol BioL 37, 61 (1973) Holbrook et of, in The Enzymes, vol. XI (part A), P. D. Boyer, Ed. (Academic Press, New York. 3rd ed 1975) pp 191-292. 

Another mechanism by which fatty acid synthesis could be inhibited in diabetic rats is a feedback inhibition of the acetyl CoA carboxylase by the longer chain length fatty acid. Fatty acid synthesis in crude liver and avocado homogenates can be blocked by adding free fatty acid or albumin-bound fatty acid to the media. But the acyl-CoA derivative of the free fatty acid rather than the free fatty acid appears to be the inhibitor. The acetyl CoA accumulation could result from the inhibition of citrate synthetase by palmityl CoA described by Lynnen. In any case diabetic ketosis is unlikely to result from retarded fatty acid synthesis because a similar and sometimes greater retardation of fatty acid synthesis is observed in starvation, and ketone body accumulation in starvation does not compare to such accumulation in diabetes. 

Diabetic ketosis where chloride is lost in the urine. 

Sodium bicarbonate given orally, dialysis for renal failure, insulin treatment for diabetic ketosis... 

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