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Dwight E Matthews

Publications and source records attributed to Dwight E Matthews.

20 records · Page 2Linked to original sources

A.S.P.E.N. 2003 Research Workshop on using tracers to measure carbohydrate, fat, and amino acid metabolism in humans.

The 2003 A.S.P.E.N. Research Workshop was held during Nutrition Week on January 18 in San Antonio, Texas. The workshop brought scientists and clinicians from around the world together to discuss the latest developments in methodology to measure substrate use and flux in vivo. Methods presented were designed to track the fate of nutrients that are given orally, enterally, or parentally to humans. Talks presented a variety of approaches to tackle particularly difficult problems of assessing intracellular processes in vivo in living animals and humans. The present paper reviews those various approaches that have been developed using (i) differential administration of tracers across organ beds to define organ-specific intracellular metabolism without tissue biopsies; (ii) animal models that will tolerate complicated multicatheter placement situations; (iii) methods that take advantage of complicated pathways of metabolism that allow movement of specific portions of a molecule for determining gluconeogenesis; (iv) nuclear magnetic resonance and in vivo magnetic resonance spectroscopy to measure intramolecular distribution of tracers; and (v) the multiple stable isotope approach to follow biosynthetic pathways associated with fatty acid flux in the fed-state in humans. Improved accessibility of these methods provides much hope for their expanded use in understanding the basic mechanisms of metabolic regulation and the physiologic changes in nutrient use that occur in disease states.

Amino Acids↗

Whole-body protein metabolism in chronic heart failure: relationship to anabolic and catabolic hormones.

BACKGROUND: Patients with chronic heart failure frequently experience profound wasting during the course of the disease, a condition termed cardiac cachexia. Although protein is the primary structural and functional component of most tissues, few studies have examined the effect of heart failure on protein metabolism. Moreover, no study has assessed the relationship of protein turnover to hormonal alterations thought to promote cachexia. Thus, our goal was to determine if whole-body protein metabolism is altered in heart failure patients and to assess the relationship of protein kinetics to circulating levels of anabolic and catabolic hormones. METHODS: We measured whole-body protein metabolism using 13C-leucine, body composition, and circulating anabolic and catabolic hormone levels in 10 patients with chronic heart failure and 11 elderly controls. RESULTS: No differences in leucine rate of appearance, oxidation, or nonoxidative disposal were noted between heart failure patients and controls. However, in a subgroup of patients characterized by increased resting energy expenditure for their metabolic body size (n = 4; > or = 20% above that predicted from fat-free mass), leucine rate of appearance (mean +/- SE; 146 +/- 6 micromol/min), an index of protein breakdown, tended to be higher compared with patients with normal resting energy expenditure (n = 5; 120 +/- 8 micromol/min) and controls (127 +/- 4 micromol/min; p = .06). Alterations in anabolic/catabolic hormone balance did not explain increased protein breakdown in this subgroup, and no correlations were found between hormone levels and protein breakdown in the heart failure group as a whole. In contrast, increased circulating interleukin-6 soluble receptor (r = 0.829; p < .01) and reduced insulin-like growth factor-I (r =-.751; p < .05) levels were related to greater rates of leucine oxidation in heart failure patients. CONCLUSION: Our results demonstrate that, although increased protein turnover is not a generalized feature of heart failure, there is a subgroup of patients characterized by resting hypermetabolism and increased protein breakdown. Moreover, hormonal alterations related to the heart failure syndrome were related to increased protein oxidation.

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