PubMed Health⌕ Search

Biomedical subjects

V Tanphaichitr

Publications and source records attributed to V Tanphaichitr.

39 records · Page 3Linked to original sources

Essential fatty acid status in adult patients receiving soybean-base formula.

Essential fatty acid (EFA) status was assessed in 48 normal Thai adults and 6 patients who required tube feeding ro 2-4 wk with commercial soybean-base formula (Sobel, Mead Johnson). Each 1000 kcal of this formula provided 40.2 g protein, 32.8 g fat, 136 g carbohydrate, 13.9 g linoleic acid, 2.9 g linolenic acid, and 0 g arachidonic acid. The linoleic acid status in these patients before receiving soybean-base formula was inadequate, as evidenced by the significantly lower serum 18:2-W6 percentage but higher serum 16:1-W7 and 18:1-W9 percentages than those in normal adults. These changes were reversed while receiving soybean-base formula. A significant positive correlation between linoleic acid intake and its serum level was demonstrated. There was a significant decrease in serum 20:4-W6 percentage while receiving soybean-base formula. This could be related to the absence of this EFA in the formula and suppression of biotransformation of 18:2-W6 to 20:4-W6 in the presence of a significant amount of 18:3-W3. None of the patients had 20:3-W9 in the serum or developed scaly dermatitis throughout the study.

Adult↗

Urinary carnitine excretion in surgical patients on total parenteral nutrition.

Urinary free and total carnitine excretions were measured in 41 normal adults and seven surgical patients on fat-free total parenteral nutrition for 8 to 45 days. The means (+/-SEM) of urinary free and total carnitine excretion in normal adults were 162 +/- 19 and 328 +/- 28 micrometers/days, respectively. All of the patients exhibited protein-calorie malnutrition with a mean carnitine intake of 11.6 +/- 1.5 micrometers/day. Under this stringent carnitine economy with the adequate supply of lysine and methionine, urinary total carnitine excretion significantly reduced to 127 to 162 micrometers/day. This probably reflects the carnitine biosynthetic rate. However, during the periods of operation and/or infection, urinary total carnitine excretion significantly increased 2- to 7-fold that of normal levels. Significant positive correlation was found between the two forms of urinary carnitine and total nitrogen excretions. Serum free and total carnitine levels in patients were significantly higher than normal adults. Such findings can be explained by the endocrine responses to the stress phenomenon and indicate a catabolic response of skeletal muscle in which most of the body carnitine resides. This can impair their carnitine status.

Adolescent↗

Carnitine metabolism and human carnitine deficiency.

Carnitine in the human body is derived from the intake of preformed dietary carnitine and biosynthesized carnitine, stemming from the metabolism of lysine and methionine. Carnitine is synthesized in liver and kidney, stored in skeletal muscle, and excreted mainly in urine. Carnitine has two main functions, i.e., transporting long-chain fatty acids into the mitochondrial matrix for beta-oxidation to provide cellular energy and modulating the rise in intramitochondrial acyl-CoA/CoA ratio, which relieves the inhibition of many intramitochondrial enzymes involving glucose and amino acid catabolism. Thus, the main consequence of carnitine deficiency is impaired energy metabolism. Human carnitine deficiency can be either hereditary or acquired. Hereditary carnitine deficiency can be grouped into three clinical entities: myopathic carnitine deficiency, systemic carnitine deficiency, and organic acidurias. Acquired carnitine deficiency is due to inadequate intake, increased requirement, and increased loss of carnitine. The definite diagnosis of carnitine deficiency is based on the determination of free- and acylcarnitine levels in serum, urine, and/or tissues. The estimated safe and adequate daily carnitine intake for adults is 150-500 mumol/day whereas pharmacological doses of carnitine are required for the treatment of hereditary carnitine deficiency.

Animals↗