Biomedical subjects

E A Medina

Publications and source records attributed to E A Medina.

4 recordsLinked to original sources

PubMed2000

Conjugated linoleic acid supplementation in humans: effects on circulating leptin concentrations and appetite.

Conjugated linoleic acid (CLA) has been demonstrated to reduce body fat in animals. However, the mechanism by which this reduction occurs is unknown. Leptin may mediate the effect of CLA to decrease body fat. We assessed the effects of 64 d of CLA supplementation (3 g/d) on circulating leptin, insulin, glucose, and lactate concentrations in healthy women. Appetite was assessed as a physiological correlate of changes in circulating leptin levels. Analysis of plasma leptin concentrations adjusted for adiposity by using fat mass as a covariate showed that CLA supplementation significantly decreased circulating leptin concentrations in the absence of any changes of fat mass. Mean leptin levels decreased over the first 7 wk and then returned to baseline levels over the last 2 wk of the study in the CLA-treated group. Appetite parameters measured at around the time when the greatest decreases in leptin levels were observed showed no significant differences between supplementation and baseline determinations in the CLA-supplemented group or between the CLA and placebo-supplemented groups. There was a nonsignificant trend for mean insulin levels to increase toward the end of the supplementation period in CLA-treated subjects. CLA did not affect plasma glucose and lactate over the treatment period. Thus, 64 d of CLA supplementation in women produced a transient decrease in leptin levels but did not alter appetite. CLA did not affect these parameters in a manner that promoted decreases of adiposity.

Adipose Tissue↗

PubMed2000

Micronutrients and innate immunity.

Micronutrients such as zinc, selenium, iron, copper, beta-carotene, vitamins A, C, and E, and folic acid can influence several components of innate immunity. Select micronutrients play an important role in alteration of oxidant-mediated tissue injury, and phagocytic cells produce reactive oxidants as part of the defense against infectious agents. Thus, adequate micronutrients are required to prevent damage of cells participating in innate immunity. Deficiencies in zinc and vitamins A and D may reduce natural killer cell function, whereas supplemental zinc or vitamin C may enhance their activity. The specific effects of micronutrients on neutrophil functions are not clear. Select micronutrients may play a role in innate immunity associated with some disease processes. Future studies should focus on issues such as age-related micronutrient status and innate immunity, alterations of micronutrients in disease states and their effect on innate immunity, and the mechanisms by which micronutrients alter innate immunity.

Deficiency Diseases↗

PubMed1999

Effects of tumor necrosis factor alpha on leptin secretion and gene expression: relationship to changes of glucose metabolism in isolated rat adipocytes.

OBJECTIVE: Our objective was to determine the effects of prolonged exposure to tumor necrosis factor-alpha (TNF-alpha) on leptin secretion from and leptin (OB) gene expression in isolated adipocytes. Because glucose uptake and the metabolism of glucose beyond lactate are important determinants of leptin production in adipocytes, we examined the effects of TNF-alpha on glucose uptake and lactate production and their relationship to leptin secretion. DESIGN AND METHODS: Isolated rat adipocytes were anchored in a defined matrix of basement membrane components and cultured with media containing 5 mM glucose, 0.16 nM insulin and several concentrations of TNF-alpha. Leptin secretion, steady-state levels of leptin mRNA levels, glucose uptake, and lactate production were assessed over 96 h. RESULTS: TNF-alpha at concentrations of 0.024, 0.24, 2.4 and 24 ng/ml did not affect leptin secretion over 24 h. TNF-alpha at concentrations of 0.24 to 24 ng/ml significantly inhibited leptin secretion over 96 h by 19-60%. TNF-alpha at concentrations of 0.024 to 24 ng/ml significantly decreased steady-state levels of leptin mRNA after 96 h by 32-95%. In addition, TNF-alpha at concentrations of 2.4 and 24 ng/ml significantly increased glucose uptake and lactate production over 96 h by 30-57%. TNF-alpha at a concentration of 0.024 ng/ml did not affect leptin secretion, glucose uptake or lactate production. Overall, for the TNF-alpha concentrations tested, leptin secretion was inversely related to the percent of glucose carbon released as lactate; however, TNF-alpha did not induce a proportional increase of lactate production from glucose. CONCLUSION: Short-term (24 h) exposure of isolated adipocytes to TNF-alpha does not affect leptin secretion. Prolonged exposure to TNF-alpha produces a concentration-dependent inhibition of leptin secretion and gene expression. This suggests that the acute effect of TNF-alpha to increase circulating leptin levels in vivo may be indirect. TNF-alpha at higher concentrations increases glucose uptake, but does not increase the conversion of glucose to lactate. Therefore, TNF-alpha appears to induce a dissociation between adipocyte glucose metabolism and leptin production.

Adipocytes↗

PubMed1986

Computer-assisted tomographic findings in a patient with African trypanosomiasis.

A 5-year-old boy was diagnosed to have trypanosomiasis and responded to treatment with diminazine. However, 22 months later symptoms recurred, with evidence of cerebral trypanosomiasis. Computer assisted tomography (CAT) scans were subsequently performed on three occasions. He was treated with melarsoprol and to date has made a full recovery. This paper reports on the evolution of the cerebral lesions shown up by the CAT scans.

Brain Diseases↗