Glucose metabolism deficiency

Like folate and vitamin C, vitamin B6 (pyroxidine) is water soluble and like folate has several vitamers. Vitamin B6 may be involved in more bodily functions than any other nutrient (Tambasco-Studart et al., 2005), is a cofactor for many enzymes, especially those involved in protein metabolism, and is also a cofactor for folate metabolism. Vitamin B6 has anticancer activity (Theodoratou et al., 2008), is a strong antioxidant (Denslow et al., 2005), is involved in hemoglobin biosynthesis, lipid and glucose metabolism and immune and nervous system function. Possible consequences of deficiency include anemia, impaired immune function, depression, confusion, and dermatitis (Spinneker et al., 2007). Vitamin B6 deficiency is generally not a problem in the developed world, but there could be as yet poorly defined consequences of suboptimal intake particularly for the elderly. 

T Diabetes mellitus, caused by a deficiency in the secretion or action of insulin, is a relatively common disease nearly 6% of the United States population shows some degree of abnormality in glucose metabolism that is indicative of diabetes or a tendency toward the condition. There are two major clinical classes of diabetes mellitus type I diabetes, or insulin-dependent diabetes mellitus (IDDM), and type II diabetes, or non-insulin-dependent diabetes mellitus (NIDDM), also called insulin-resistant diabetes. 

CHROMIUM Enhances the effect of insulin. Deficiency—results in defective glucose metabolism. Excess—occurs in chronic inhalation of chromium dust and may lead to carcinoma of the lung. 

Cr(in) is essential— deficiencies result in defective glucose metabolism, hyperlipidemia, comeal opacity... 

Ketogenesis is an important metabolic function in the liver. It is the result of an increase in lipolysis in the fatty tissue, with a rise in fatty acids. Insulin inhibits ketogenesis, whereas it is accelerated by fasting as well as by glucagons and insulin deficiency. Ketones (acetacetate, 3-hydroxybutyrate, acetone) are synthesized by means of P-oxidation from acetyl-CoA, assuming the production of this substance exceeds the amount required by the hepa-tocytes (and glucose metabolism is simultaneously reduced). The liver itself does not require any ketones acetone is expired, whereas 3-hydroxybutyrate and acetacetate serve as a source of energy. Ketonaemia can lead to metabolic acidosis and electrolyte shifts. 

Chromium is a trivalent cption that occurs as A typical daily intake isO-5 3-8 jimoJ (25-200 ig/day). After absorption from the diet, chromium occurs bound to transferrin. A safe and adequate intake of 50 to 200 ffg Cr/day has been established. Chromium appears to participate in glucose metabolism. The ion may play a part in mediating the hormonal effects of insulin. Chromium deficiency results in abnormally high glucose tolerance curves and impaired clearance of plasma glucose. Chromium deficiency can be induced in animals. There is evidence that... 

Figure 5-29. Conversion of galactose to intermediates of glucose metabolism. Galactose 1-phosphate uridyl transferase is deficient in classic galactosemia.

As noted above, there have been reports that link some cases of APLP with a defect in fatty acid metabolism in the fetus. These include fetal deficiencies of long chain 3-hydroxyacyl-coenzyme A dehydrogenase (LCHAD), carnitine-palmitoyl transferase 1 (CPT 1), and medium chain acyl-coenzyme A dehydrogenase (MCAD). The mechanism by which defective fetal fatty acid oxidation causes maternal illness is not known. However, since the fetus uses primarily glucose metabolism for its energy needs, it is likely that toxic products from the placenta, which does use fatty acid oxidation, cause the maternal liver failure. 

Glucose metabolism in the ebb phase of the response to trauma— a raised blood glucose and reduced tissue glucose utilization—are similar to those expected in insulin deficiency. However, direct measurement of plasma insulin by an immunological method shows plasma insulin levels to be increased after moderately severe surgery (R9). 

Finally, perhaps an explanation for the beneficial effects of coenzyme A (CoA), malate and pyruvate for the extracellular in vitro growth of P. lophurae found by Trager (1952) and interpreted by Moulder (1962) to neatly explain the shift in pattern of carbohydrate metabolism accompanying liberation of parasites from the host cell. .. (The) lack of CoA in free parasites logically explains the lessened rate of pyruvic acid oxidation via the Krebs cycle. It is difficult to escape the conclusion that the inability of plasmodia to synthesize CoA extracellularly results in extensive dislocations in glucose metabolism, which in turn contribute heavily to the restriction of the malarial parasite to an intracellular habitat is this malate and pyruvate could be linked to the generation of dihydronicotinamide adenine dinucleotide (NADH) for glycolysis, and a CoA deficiency could limit activity in pathways other than the TCA cycle. 

What effect will carnitine deficiency have on p-oxidation What effect will carnitine deficiency have on glucose metabolism ... 

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