Intolerance carbohydrate

Common but usually transient side effects are lethargy, incoordination, blurred vision, higher cortical dysfunction, and drowsiness. At concentrations greater than 50 mcg/mL, phenytoin can exacerbate seizures. Chronic side effects include gingival hyperplasia, impaired cognition, hirsutism, vitamin D deficiency, osteomalacia, folic acid deficiency, carbohydrate intolerance, hypothyroidism, and peripheral neuropathy. 

The KIGS/KIMS (Pharmacia International Growth Database) has reported 233 patients with Prader-Willi syndrome, of whom three developed carbohydrate intolerance. 

Woolliscroft J, Barbosa J. 1977. Analysis of chromium induced carbohydrate intolerance in the rat. J Nutr 107(9) 1702-1706. 

Carbohydrate intolerance is caused by those diuretics which produce prolonged hypokalaemia, i.e. the loop and thiazide type. It appears that intracellular potassium is necessary for the formation of insulin, and glucose intolerance is probably due to insulin deficiency. Insulin requirements thus increase in established diabetics and the disease may become mainifest in latent diabetics. The effect is generally reversible over several months. 

The presence of the brush-border disaccharidases is essential for carbohydrate absorption, and a reduction in their activity leads to carbohydrate malabsorption and intolerance. Carbohydrate malabsorption does not always lead to chnical symptoms, but when symptoms do occur (e.g., abdominal pam, flatulence, and diarrhea) as a consequence of the malabsorption, the patient is described as having carbohydrate intolerance. 

Because of the lipase deficiency, fat-soluble vitamin (A, D, E, and K) deficiencies may occur. Whether lipase activity or bile acids (e.g., in micelle formation) are involved in fat-soluble vitamin absorption with steatorrhea is unclear. Vitamin and zinc deficiencies also may occur as aresult of pancreatic enzyme deficiency. Although pancreatic involvement is predominantly exocrine in nature, insulin deficiency with glucose intolerance also occurs in CF patients, especially as they advance in age. Carbohydrate intolerance is characterized by low insulin concentrations and enhanced peripheral sensitivity to insulin but not by the presence of islet cell or anti-insulin antibodies. Carbohydrate intolerance in CF is not usually associated with the ketosis as commonly occurs in type 1 diabetes. This complication involves an increase in the number of insulin receptors with decreased affinity for insulin. Despite a concomitant increase in tissue affinity for insulin, 8% of CF children over 12 years of age require insulin therapy. 

None of the subjects that we report have carbohydrate intolerance and to our knowledge glycosylated hemoglobin has not been evaluated in normoglycemic patients on fiber diets. 

Aspects of chemical methods used in the structural elucidation of polysaccharides and complex carbohydrates have been reviewed. In a critical examination of the use of g.l.c.-m.s. in the identification of TMS ethers of monosaccharides, a standardized method, which uses a medium resolution mass spectrometer and short chromatographic columns, has been proposed. TMS Ethers of monosaccharides have been characterized by g.l.c.-chemical ionization m.s. with ammonia as reagent gas. Molecular weights were determined, and fragment ions were produced in a quantity high enough to differentiate between stereoisomers (epimers and anomers). Disaccharides have been determined by permethylation followed by g.l.c. The method has been used in the detection of carbohydrate intolerance secondary to intestinal disaccharidase deficiency. 

Fredrickson and Lees (1965) have described as their type III hyperlipoproteinemia, individuals who, in addition to clinical and laboratory evidence of essential hypercholesterolemia, show elevation of VLDLP (pre-j8-lipoproteins) and are markedly susceptible to carbohydrate induction. In common with other endogenous hyperlipidemics, they manifest carbohydrate intolerance. 

The possible relationship between overt and occult carbohydrate intolerance in endogenous hyperlipemias and the development of premature atherosclerosis remains to be evaluated. 

Also see INBORN ERRORS OF METABOLISM, Table 1-2, Inborn Errors of Carbohydrate Metabolism, "Carbohydrate Intolerance.")... 

These Macaca nigra are maintained on much the same kind of diet as are other monkey species at the Oregon Primate Center and in most other institutions, yet other species apparently do not develop the diabetic syndrome. There have been several reports of spontaneous atherosclerosis in nonhuman primates that were not challenged with atherogenic diets (8-14). Carbohydrate intolerance and possible diabetes were reported in squirrel monkeys (15) some of which also exhibited atherosclerosis. However, this report directly relates the degree and severity of atherosclerosis to the intensity of the clinical syndrome of diabetes mellitus in each of the monkeys. 

In the women with vitamin Bg deficiency, administration of this vitamin caused elevation of fasting blood-pyruvate levels, and reduction of plasma glucose, insulin, and blood-pyruvate responses after an oral glucose load. These changes were not found in the 28 non-vitamin Bg-deficient women. These results indicate that carbohydrate intolerance in women on oral contraceptives is... 

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