Body composition and dietary intake in neoplastic disease

Cohn, S. H.; Gartenhaus, W; Vartsky, D.; Sawitsky, Arthur; Zanzi, I.; Vaswani, A.; Yasumura, S; Rai, Kanti; Cortés, Ernesto; Ellis, Kenneth J.

doi:10.1093/ajcn/34.10.1997

Cited by 78 publications

(27 citation statements)

References 6 publications

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“…The rate of [1][2][3][4][5][6][7][8][9][10][11][12][13] C]glucose incorporation into C1 glycogen was linear in both groups (IDDM subjects, r ϭ 0.944Ϯ0.031; controls, r ϭ 0.978Ϯ0.009) and the net rates of muscle glycogen synthesis were calculated to be 108Ϯ16 mol/liter of muscle per minute in the IDDM group and 195Ϯ6 mol/liter of muscle per minute in the control group (P Ͻ 0.001). Assuming that muscle mass is equivalent to 26% body weight (14), net muscle glycogen synthesis could account for 76Ϯ16% and 69Ϯ17% of nonoxidative glucose metabolism in the IDDM and control subjects, respectively (Table I).…”

Section: Resultsmentioning

confidence: 99%

Mechanism of impaired insulin-stimulated muscle glucose metabolism in subjects with insulin-dependent diabetes mellitus.

Cline¹,

Magnusson²,

Rothman³

et al. 1997

J. Clin. Invest.

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To determine the mechanism of impaired insulin-stimulated muscle glycogen metabolism in patients with poorly controlled insulin-dependent diabetes mellitus (IDDM), we used 13 C-NMR spectroscopy to monitor the peak intensity of the C1 resonance of the glucosyl units in muscle glycogen during a 6-h hyperglycemic-hyperinsulinemic clamp using [1-13 C]glucose-enriched infusate followed by nonenriched glucose. Under similar steady state ( t ϭ 3-6 h) plasma glucose ( ‫ف‬ 9.0 mM) and insulin concentrations ( ‫ف‬ 400 pM), nonoxidative glucose metabolism was significantly less in the IDDM subjects compared with age-weight-matched control subjects (37 Ϯ 6 vs. 73 Ϯ 11 mol/kg of body wt per minute, P Ͻ 0.05), which could be attributed to an ‫ف‬ 45% reduction in the net rate of muscle glycogen synthesis in the IDDM subjects compared with the control subjects (108 Ϯ 16 vs. 195 Ϯ 6 mol/liter of muscle per minute, P Ͻ 0.001). Muscle glycogen turnover in the IDDM subjects was significantly less than that of the controls (16 Ϯ 4 vs. 33 Ϯ 5%, P Ͻ 0.05), indicating that a marked reduction in flux through glycogen synthase was responsible for the reduced rate of net glycogen synthesis in the IDDM subjects. 31 P-NMR spectroscopy was used to determine the intramuscular concentration of glucose-6-phosphate (G-6-P) under the same hyperglycemic-hyperinsulinemic conditions. Basal G-6-P concentration was similar between the two groups ( ‫ف‬ 0.10 mmol/kg of muscle) but the increment in G-6-P concentration in response to the glucose-insulin infusion was ‫ف‬ 50% less in the IDDM subjects compared with the control subjects (0.07 Ϯ 0.02 vs. 0.13 Ϯ 0.02 mmol/kg of muscle, P Ͻ 0.05). When nonoxidative glucose metabolic rates in the control subjects were matched to the IDDM subjects, the increment in the G-6-P concentration (0.06 Ϯ 0.02 mmol/kg of muscle) was no different than that in the IDDM subjects. Together, these data indicate that defective glucose transport/phosphorylation is the major factor responsible for the lower rate of muscle glycogen synthesis in the poorly controlled insulin-dependent diabetic subjects. ( J. Clin. Invest. 1997. 99:2219-2224.)

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Section: Resultsmentioning

confidence: 99%

Mechanism of impaired insulin-stimulated muscle glucose metabolism in subjects with insulin-dependent diabetes mellitus.

Cline¹,

Magnusson²,

Rothman³

et al. 1997

J. Clin. Invest.

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“…The Ra of palmitic acid and glycerol in plasma were calculated by the equation described by Steele (30 (2) Ra is the rate of appearance of glycerol or palmitic acid in ,gmol * kg-' -min-', IEj is the isotopic enrichment ofthe infusate (mole percent excess), and IEp is the isotopic enrichment of plasma (mole percent excess) at isotopic equilibrium.…”

Section: Methodsmentioning

confidence: 99%

“…During the course of their illness, patients with cancer often lose weight, depleting body protein and fat (1,2). Understanding the mechanisms involved in loss of body fat may be clinically important because weight loss itself is a bad prognostic sign (3,4) and the amount of remaining fat in starved individuals has been shown to correlate closely with the duration of survival (5).…”

Section: Introductionmentioning

confidence: 99%

Whole-body lipolysis and triglyceride-fatty acid cycling in cachectic patients with esophageal cancer.

Klein

Wolfe²

1990

J. Clin. Invest.

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Whole-body lipolytic rates and the rate of triglyceride-fatty acid cycling (reesterification of fatty acids released during Iipolysis) were measured with stable isotopic tracers in the basal state and during,8-adrenergic blockade with propranolol infusion in five cachectic patients with squamous cell carcinoma of the esophagus, five cachectic cancer-free, nutritionallymatched control patients, and 10 healthy volunteers. Resting energy expenditure and plasma catecholamines were normal in all three groups. The basal rate of glycerol appearance in blood in the patients with cancer (2.96±0.45 gmol -kg-' * min-') was similar to that in the nutritionally matched controls (3.07±0.28iumol -kg-' -min-'), but 48% greater than in the normal-weight volunteers (2.00±0.16 ;smol * kg-' * min-') (P = 0.028). The antilipolytic effect of propranolol and the rate of triglyceridefatty acid cycling in the patients with cancer were also similar in the cachectic control group and -50% greater than in the normal-weight volunteers, but the differences were not statistically significant because of the variability in the data.We conclude that the increase in lipolysis and triglyceride-fatty acid cycling in "unstressed" cachectic patients with esophageal cancer is due to alterations in their nutritional status rather than the presence of tumor itself. Increased ,Badrenergic activity may be an important contributor to the stimulation of lipolysis. (J. Clin.

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“…Warnold et al 10 reported a mean energy intake of 1,270 kcal/day in 29 cancer patients, which, although varying greatly, was not significantly different from healthy controls. Cohn et al 13 assessed energy and protein intake related to lean body mass in 22 oncological patients and found it to be not different from 8 normal subjects, except in 6 weight-losing patients with solid tumors, where intake was lower. Bennegård et al, 14 using a 3-day food record, found a spontaneous daily food energy intake of 26.3 Ϯ 2.4 kcal/kg in 8 weight-losing cancer patients, very similar to the present results.…”

Section: Hypermetabolismmentioning

confidence: 99%

Dietary intake and resting energy expenditure in relation to weight loss in unselected cancer patients

et al. 2001

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Weight loss and anorexia are frequent findings in advanced cancer. The progressive wasting could be attributed to changes in dietary intake and/or energy expenditure mediated by metabolic alterations. In this study, we analyzed dietary intake in generalized malignant disease of solid tumor type in relation to resting energy expenditure (REE) and reported weight loss. In a group of 297 unselected cancer patients from a university hospital outpatient clinic, dietary intake of energy and macronutrients from a 4-day food record, REE by indirect calorimetry, height, weight and weight loss were recorded. Protein intake was validated against 24 hr urine nitrogen in a subgroup (n ‫؍‬ 53), and no indication of systematic misreporting was found. Mean daily dietary intake was below maintenance requirements, 26 ؎ 10 kcal/kg. Weight loss of more than 10% was present in 43% of patients and elevated REE (>110% of predicted) in 48%. Dietary intake did not differ between normo-and hypermetabolic patients, nor was tumour type or gender related to energy and protein intake. Weight loss could not be accounted for by diminished dietary intake since energy intake in absolute amounts was not different and intake per kilogram body weight was higher in weight-losing patients compared to weight-stable patients. Dietary macronutrient composition did not differ from the general population. Dietary intake of energy and protein was decreased, but dietary macronutrient composition did not appear to be changed. Weight loss and hypermetabolism were frequent and not compensated for by an increase in spontaneous food intake. Our results indicate that an expected up-regulation of dietary intake in response to elevated energy expenditure is frequently lost in cancer patients. This may be the explanation behind cancer cachexia rather than a primary decrease in appetite.

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Body composition and dietary intake in neoplastic disease

Cited by 78 publications

References 6 publications

Mechanism of impaired insulin-stimulated muscle glucose metabolism in subjects with insulin-dependent diabetes mellitus.

Mechanism of impaired insulin-stimulated muscle glucose metabolism in subjects with insulin-dependent diabetes mellitus.

Whole-body lipolysis and triglyceride-fatty acid cycling in cachectic patients with esophageal cancer.

Dietary intake and resting energy expenditure in relation to weight loss in unselected cancer patients

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