Insulin resistance in patients with cancer: relationships with tumor site, tumor stage, body-weight loss, acute-phase response, and energy expenditure

Nutrition ◽  
2001 ◽  
Vol 17 (7-8) ◽  
pp. 590-593 ◽  
Author(s):  
Takaki Yoshikawa ◽  
Yoshikazu Noguchi ◽  
Chiharu Doi ◽  
Tatsuo Makino ◽  
Katsutoshi Nomura
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Body Weight ◽  
Energy Expenditure ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Body Weight Loss ◽  
Tumor Stage ◽  
Tumor Site ◽  
Patients With Cancer

scholarly journals Leptin produces anorexia and weight loss without inducing an acute phase response or protein wasting

1998 ◽  
Vol 274 (6) ◽  
pp. R1518-R1525 ◽  
Author(s):  
Atsushi Kaibara ◽  
Armin Moshyedi ◽  
Troy Auffenberg ◽  
Amer Abouhamze ◽  
Edward M. Copeland ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Acute Phase Protein ◽  
Obese Mice ◽  
Preferential Loss ◽  
Phase Protein ◽  
Protein Response

The ob gene product leptin is known to produce anorexia and loss of body fat when chronically administered to both lean and genetically obese mice. The current study was undertaken to examine whether administration of recombinant leptin in quantities sufficient to produce decreases in food intake and body weight and alterations in body composition would elicit either an hepatic acute phase protein response or preferential loss of carcass lean tissue. Mice were administered increasing quantities of recombinant human leptin or human tumor necrosis factor-α as a positive control. Although leptin (at 10 mg/kg body wt) produced significant anorexia and weight loss (both P < 0.05), human leptin administration did not appear to induce an hepatic acute phase protein response in either lean or genetically obese mice, as determined by protein synthetic rates in the liver or changes in the plasma concentration of the murine acute phase protein reactants, amyloid A, amyloid P, or seromucoid (α1-acid glycoprotein). In addition, human leptin administration did not induce a loss of fat-free dry mass (protein) in lean or obese animals. The findings suggest that at doses adequate to alter food intake and body weight leptin is not a significant inducer of the hepatic acute phase response nor does leptin promote the preferential loss of somatic protein characteristic of a chronic inflammatory process.

High-fat diet induces site-specific unresponsiveness to LPS-stimulated STAT3 activation in the hypothalamus

2014 ◽  
Vol 306 (1) ◽  
pp. R34-R44 ◽  
Author(s):  
Beatriz de Carvalho Borges ◽  
Rodrigo Rorato ◽  
Ernane Torres Uchoa ◽  
Paula Marangon ◽  
Glauber S. F. da Silva ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Brain Stem ◽  
High Fat Diet ◽  
Control Diet ◽  
Body Weight Loss ◽  
Hypothalamic Nucleus ◽  
High Fat

Hypophagia induced by inflammation is associated with Janus kinase (JAK)-2/signal transducer and activator of transcription (STAT) 3 signaling pathway, and leptin-mediated hypophagia is also mediated by JAK2-STAT3 pathway. We have previously reported that lipopolysaccharide (LPS) did not reduce food intake in leptin-resistant high-fat diet (HFD) rats but maintained body weight loss. We investigated whether changes in p-STAT3 expression in the hypothalamus and brain stem could account for the desensitization of hypophagia in HFD animals after a low LPS dose (100 μg/kg). Wistar rats fed standard diet (3.95 kcal/g) or HFD (6.3 kcal/g) for 8 wk were assigned into control diet-saline, control diet-LPS, HFD-saline, and HFD-LPS groups. LPS reduced feeding in the control diet but not HFD. This group showed no p-STAT3 expression in the paraventricular nucleus (PVN) and ventromedial hypothalamic nucleus (VMH), but sustained, though lower than control, p-STAT3 in the nucleus of the solitary tract (NTS) and raphe pallidus (RPa). LPS decreased body weight in HFD rats and increased Fos expression in the NTS. LPS increased body temperature, oxygen consumption, and energy expenditure in both control diet and HFD rats, and this response was more pronounced in HFD-LPS group. Brown adipose tissue (BAT) thermogenesis and increased energy expenditure seem to contribute to body weight loss in HFD-LPS. This response might be related with increased brain stem activation. In conclusion, LPS activates STAT3-mediated pathway in the hypothalamus and brain stem, leading to hypophagia, however, LPS effects on food intake, but not body weight loss, are abolished by leptin resistance induced by HFD. The preserved STAT3 phosphorylation in the brain stem suggests that unresponsiveness to LPS on STAT3 activation under HFD might be selective to the hypothalamus.

Postprandial insulin sensitivity and thermogenesis in frail elderly women

2010 ◽  
Vol 35 (4) ◽  
pp. 526-533 ◽  
Author(s):  
Eric D.B. Goulet ◽  
Zareen Khursigara ◽  
Réjeanne Gougeon ◽  
José A. Morais
Keyword(s):  
Physical Activity ◽  
Insulin Resistance ◽  
Weight Loss ◽  
Body Weight ◽  
Insulin Sensitivity ◽  
Frail Elderly ◽  
Elderly Women ◽  
Body Weight Loss ◽  
Healthy Elderly ◽  
Postprandial Insulin

The frailty syndrome is associated with inflammation, hypercortisolemia, and cardiovascular diseases, all of which are linked with insulin resistance. But whether frailty is characterized by insulin resistance is unclear, especially in the postprandial state. The prevalence of underweight with frailty is high. We wondered whether hypermetabolism associated with inflammation and hypercortisolemia could increase the thermic effect of food (TEF) and contribute to the frailty-associated body weight loss. In this study, we determined whether insulin sensitivity and TEF responses differ between frail and healthy elderly persons following a meal. Ten healthy and 13 frail elderly women were recruited and studied during the 5 h following the ingestion of a standardized liquid mixed-meal test. Areas under the curve (AUC) for glucose and insulin, and the product of AUC glucose × AUC insulin × 10−6 (PGI) were used as indices of insulin sensitivity. TEF was measured by indirect calorimetry. Following the meal, glucose and insulin AUCs and PGI were significantly higher in frail than in healthy elderly women and, except for the insulin AUC; these differences remained significant after adjustment for age, body weight, and physical activity. Physical activity, determined by questionnaire, was the single best predictor of PGI, explaining 27% of its variance. There was no difference in TEF between groups, and it did not correlate with any significant variable measured. Our results suggest that postprandial insulin resistance is higher in frail than in healthy elderly women, and TEF is similar, indicating that both processes do not contribute to the propensity for body weight loss.

Effect of ibuprofen on the acute-phase response and protein metabolism in patients with cancer and weight loss

1995 ◽  
Vol 82 (2) ◽  
pp. 229-234 ◽  
Author(s):  
T. Preston ◽  
K. C. H. Fearon ◽  
D. C. McMillan ◽  
F. P. Winstanley ◽  
C. Slater ◽  
...  
Keyword(s):  
Weight Loss ◽  
Acute Phase ◽  
Protein Metabolism ◽  
Acute Phase Response ◽  
Phase Response ◽  
Patients With Cancer

Greater than predicted decrease in energy expenditure during exercise after body weight loss in obese men

2003 ◽  
Vol 105 (1) ◽  
pp. 89-95 ◽  
Author(s):  
Eric DOUCET ◽  
Pascal IMBEAULT ◽  
Sylvie ST-PIERRE ◽  
Natalie ALMÉRAS ◽  
Pascale MAURIÈGE ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Energy Expenditure ◽  
Body Weight Loss

Weight loss and low body cell mass in males with lung cancer: relationship with systemic inflammation, acute-phase response, resting energy expenditure, and catabolic and anabolic hormones

1999 ◽  
Vol 97 (2) ◽  
pp. 215-223 ◽  
Author(s):  
Jean Paul F. H. A. SIMONS ◽  
Annemie M. W. J. SCHOLS ◽  
Wim A. BUURMAN ◽  
Emiel F. M. WOUTERS
Keyword(s):  
Lung Cancer ◽  
Weight Loss ◽  
Energy Expenditure ◽  
Acute Phase ◽  
Systemic Inflammation ◽  
Acute Phase Response ◽  
Resting Energy Expenditure ◽  
Phase Response ◽  
Igf I ◽  
Circulating Levels

The aim of the present study was to investigate, in human lung cancer, the relationship between weight loss and the existence of a low body cell mass (BCM) on the one hand, and the putative presence of systemic inflammation, an increased acute-phase response, anorexia, hypermetabolism and changes in circulating levels of several anabolic and catabolic hormones on the other. In 20 male lung cancer patients, pre-stratified by weight loss of ⩾ 10% (n = 10) or of < 10% (n = 10), the following measurements were performed: BCM (by dual-energy X-ray absorptiometry/bromide dilution), circulating levels of sTNF-R55 and sTNF-R75 (soluble tumour necrosis factor receptors of molecular masses 55 and 75 kDa respectively), interleukin-6, lipopolysaccharide-binding protein, albumin, appetite (scale of 0–10), resting energy expenditure (by indirect calorimetry) and circulating levels of catabolic (cortisol) and anabolic [testosterone, insulin-like growth factor-I (IGF-I)] hormones. Compared with the patients with a weight loss of < 10%, those with a weight loss of ⩾ 10% were characterized by higher levels of sTNF-R55 (trend towards significance; P = 0.06), and lower levels of albumin (27.4 compared with 34.4 mmol/l; P = 0.02), testosterone (13.2 compared with 21.5 nmol/l; P = 0.01) and IGF-I (119 compared with 184 ng/ml; P = 0.004). In the patient group as a whole, the percentage weight loss was significantly correlated with sTNF-R55 (r = 0.59, P = 0.02), albumin (r =-0.63, P = 0.006) and IGF-I (r =-0.50, P = 0.02) levels. Height-adjusted BCM was significantly correlated with sTNF-R55 (r =-0.57, P = 0.03), sTNF-R75 (r =-0.50, P = 0.04), lipopolysaccharide-binding protein (r =-0.50, P = 0.04), albumin (r = 0.56, P = 0.02) and resting energy expenditure/BCM (r =-0.54, P = 0.03), and there was a trend towards a correlation with IGF-I concentration (r = 0.44, P = 0.06). We conclude that, in human lung cancer, weight loss and the presence of a low BCM are associated with systemic inflammation, an increased acute-phase response and decreased levels of IGF-I. In addition, a decreased BCM is associated with hypermetabolism.

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