The American journal of clinical nutrition
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L-Arginine is an important precursor of nitric oxide (NO) and protein synthesis. Arginine is produced in the body (mainly kidney) by de novo production from citrulline and by protein breakdown. Arginine availability appears to be limited in sepsis. ⋯ Citrulline production is severely low in patients with sepsis and is related to diminished de novo arginine and NO production. These metabolic alterations contribute to reduced citrulline and arginine availability, and these findings warrant further studies of therapeutic nutritional interventions to restore arginine metabolism in sepsis.
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Consumption of sugar-sweetened beverages (SSBs) has been linked to obesity and type 2 diabetes. ⋯ Over the past decade, US adult SSB consumption has increased. SSB comprises a considerable source of total daily intake and is the largest source of beverage calories. SSB consumption is highest among subgroups also at greatest risk of obesity and type 2 diabetes.
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The glycemic index (GI) characterizes foods by using the incremental area under the glycemic response curve relative to a similar amount of oral glucose. Its ability to differentiate between curves of different shapes, the peak response, and other aspects of the glycemic response is debatable. ⋯ The GI provides a good summary of postprandial glycemia. It predicts the peak (or near peak) response, the maximum glucose fluctuation, and other attributes of the response curve.
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Previous trials suggest that oral l-arginine administration affects endothelial function. However, most of these studies were small, the conclusions were inconsistent, and the precise effects are therefore debatable. ⋯ Short-term oral l-arginine is effective at improving the fasting vascular endothelial function when the baseline FMD is low.
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Review
Regulation of skeletal muscle mitochondrial fatty acid metabolism in lean and obese individuals.
A reduction in fatty acid (FA) oxidation has been associated with lipid accumulation and insulin resistance in skeletal muscle of obese individuals. Numerous reports suggest that the reduction in FA oxidation may result from intrinsic mitochondrial defects, although little direct evidence has been offered to support this conclusion. This brief review summarizes recent work from our laboratory that reexamined whether this decrease in skeletal muscle FA oxidation with obesity was attributable to a dysfunction in FA oxidation within mitochondria or simply to a reduction in muscle mitochondrial content. ⋯ However, this did not result from decreased protein contents of various transcription factors, because peroxisome proliferater-activated receptor gamma coactivator 1alpha (PGC1alpha), PGC1beta, peroxisome proliferator-activated receptor alpha (PPARalpha), and mitochondrial transcription factor A (TFAM) were not reduced with obesity. In contrast, it appears that obesity is associated with altered regulation of cofactors (PGC1alpha and PGC1beta) and their downstream transcription factors (PPARalpha, PPARdelta/beta, and TFAM), because relations among these variables were present in muscle from lean individuals but not from obese individuals. These findings imply that obese individuals would benefit from interventions that increase the skeletal muscle mitochondrial content and the potential for oxidizing FAs.