Oxygen isotope ratios in primate bone carbonate reflect amount of leaves and vertical stratification in the diet.

The stable isotopic biogeochemistry of free-ranging primates is a unique tool to assess dietary and ecological adaptions among sympatric populations. The present study tested the hypothesis that oxygen isotopes in the bone carbonate of five primate and four ungulate species that live in Kibale National Park, Uganda, would show minimal variability since the species obtain water from a single water source. Bones were analyzed for stable carbon (δ(13) C) and oxygen (δ(18) O) isotope ratios.

Molecular modeling and functional confirmation of a predicted fatty acid binding site of mitochondrial aspartate aminotransferase.

Molecular interactions are necessary for proteins to perform their functions. The identification of a putative plasma membrane fatty acid transporter as mitochondrial aspartate aminotransferase (mAsp-AT) indicated that the protein must have a fatty acid binding site. Molecular modeling suggests that such a site exists in the form of a 500-Å(3) hydrophobic cleft on the surface of the molecule and identifies specific amino acid residues that are likely to be important for binding.

Increased hepatocellular uptake of long chain fatty acids occurs by different mechanisms in fatty livers due to obesity or excess ethanol use, contributing to development of steatohepatitis in both settings.

Long chain fatty acids (LCFA) enter cells by both facilitated transport and diffusion, the former accounting for > or = 90%. Facilitated LCFA transport is up-regulated in adipocytes from obese rats, mice, and humans. To clarify the role of hepatocellular LCFA uptake in hepatic steatosis (fatty liver), [3H]-oleic acid (OA) uptake was studied in hepatocytes isolated from Zucker fatty(Z) and control(C) and ethanol-fed(E) Wistar rats, and demonstrated both saturable and non-saturable components, each a function of the unbound OA concentration ([OAu]).

Lipid metabolism and liver inflammation. I. Hepatic fatty acid uptake: possible role in steatosis.

Hepatic steatosis is a growing public health concern. Nonalcoholic fatty liver is increasingly common in Western societies and may lead to steatohepatitis, fibrosis, and cirrhosis, possibly triggered by lipid peroxidation. The relation of fatty liver to obesity, type II diabetes, and/or metabolic syndrome is significant.

Lipid metabolism in hepatic steatosis.

Hepatic steatosis is a consequence of both obesity and ethanol use. Nonalcoholic steatosis (NASH) resemble alcoholic steatosis and steatohepatitis. Both exhibit increased hepatocellular triglycerides(TG), reflecting an increase in long chain fatty acids (LCFA).

Leptin and insulin modulate nutrient partitioning and weight loss in ob/ob mice through regulation of long-chain fatty acid uptake by adipocytes.

Leptin treatment of ob/ob mice leads to weight loss appreciably greater than that in pair-fed mice. To test whether this "extra" weight loss is mediated by leptin-induced alterations in nutrient partitioning, the effects in ob/ob mice of subcutaneous leptin infusion (500 ng/h for View Article and Find Full Text PDF