Teaching the Nutrition Focused Physical Exam (NFPE) To Medical Students Using an Interdisciplinary Approach.

Nutritional status greatly affects the health of patients, yet the time devoted to nutrition curriculum in medical school is minimal. We implemented a novel approach of teaching the Nutrition Focused Physical Exam (NFPE) as a tool to demonstrate the importance of assessing the nutritional status of patients and learning about malnutrition and nutrient deficiencies.

Effects of HIV and antiretroviral therapy on resting energy expenditure in adult HIV-infected women-a matched, prospective, cross-sectional study.

BACKGROUND: Several studies have reported increased resting energy expenditure (REE) in people with human immunodeficiency virus (HIV). However, limited data exist on REE in HIV-infected women and the effect of antiretroviral therapy (ART) on REE in this population. OBJECTIVE: The purpose of this study was to compare REE in healthy controls to adult HIV-infected women classified in three groups: naïve to ART, on ART with virologic suppression, and on ART with an HIV-1 RNA level >5,000 copies/mL. DESIGN: After a fast, body composition by bioelectrical impedance analysis and REE by indirect calorimetry were determined. Anthropometric measures were also taken. STATISTICAL ANALYSIS: Distributionally appropriate two-sample tests were used for between-group analyses and analysis of covariance was used for confounding adjustment. RESULTS: Eighty-seven women were enrolled and the HIV-infected and control women were matched for age and body mass index. Log-transformed REE was significantly higher in HIV-infected women naïve to ART compared to controls (7.26±0.22 vs 7.14±0.19; P=0.04, respectively) and the difference remained significant after adjustment for body cell mass (P=0.008). Log-transformed REE was not different in HIV-infected women on ART compared to HIV-infected women naïve to ART (7.25±0.25 vs 7.26±0.23; P=0.81, respectively). Adjusting for body cell mass did not change the results (P=0.56). Similarly, REE was not different between women naïve to ART and those on ART with undetectable HIV-1 RNA, regardless of adjustment for body cell mass. REE correlated to current and nadir CD4 count and trended toward a negative correlation with HIV-1 RNA levels. CONCLUSIONS: We showed that REE is elevated in ART-naïve, HIV-infected women and continues to be elevated when on ART, regardless of virologic suppression, compared to age and body mass index-matched healthy women. This suggests an effect of HIV infection itself and not ART on REE in these HIV-infected women, and should be considered during nutrition assessment and counseling of HIV-infected adult women.

Metabolomics and mass isotopomer analysis as a strategy for pathway discovery: pyrrolyl and cyclopentenyl derivatives of the pro-drug of abuse, levulinate.

We recently reported that levulinate (4-ketopentanoate) is converted in the liver to 4-hydroxypentanoate, a drug of abuse, and that the formation of 4-hydroxypentanoate is stimulated by ethanol oxidation. We also identified 3 parallel ß-oxidation pathways by which levulinate and 4-hydroxypentanoate are catabolized to propionyl-CoA and acetyl-CoA. We now report that levulinate forms three seven-carbon cyclical CoA esters by processes starting with the elongation of levulinyl-CoA by acetyl-CoA to 3,6-diketoheptanoyl-CoA. The latter γ-diketo CoA ester undergoes two parallel cyclization processes. One process yields a mixture of tautomers, i.e., cyclopentenyl- and cyclopentadienyl-acyl-CoAs. The second cyclization process yields a methyl-pyrrolyl-acetyl-CoA containing a nitrogen atom derived from the ε-nitrogen of lysine but without carbons from lysine. The cyclic CoA esters were identified in rat livers perfused with levulinate and in livers and brains from rats gavaged with calcium levulinate ± ethanol. Lastly, 3,6-diketoheptanoyl-CoA, like 2,5-diketohexane, pyrrolates free lysine and, presumably, lysine residues from proteins. This may represent a new pathway for protein pyrrolation. The cyclic CoA esters and related pyrrolation processes may play a role in the toxic effects of 4-hydroxypentanoate.

Metabolism of levulinate in perfused rat livers and live rats: conversion to the drug of abuse 4-hydroxypentanoate.

Calcium levulinate (4-ketopentanoate) is used as an oral and parenteral source of calcium. We hypothesized that levulinate is converted in the liver to 4-hydroxypentanoate, a new drug of abuse, and that this conversion is accelerated by ethanol oxidation. We confirmed these hypotheses in live rats, perfused rat livers, and liver subcellular preparations. Levulinate is reduced to (R)-4-hydroxypentanoate by a cytosolic and a mitochondrial dehydrogenase, which are NADPH- and NADH-dependent, respectively. A mitochondrial dehydrogenase or racemase system also forms (S)-4-hydroxypentanoate. In livers perfused with [(13)C(5)]levulinate, there was substantial CoA trapping in levulinyl-CoA, 4-hydroxypentanoyl-CoA, and 4-phosphopentanoyl-CoA. This CoA trapping was increased by ethanol, with a 6-fold increase in the concentration of 4-phosphopentanoyl-CoA. Levulinate is catabolized by 3 parallel pathways to propionyl-CoA, acetyl-CoA, and lactate. Most intermediates of the 3 pathways were identified by mass isotopomer analysis and metabolomics. The production of 4-hydroxypentanoate from levulinate and its stimulation by ethanol is a potential public health concern.