Tumor Necrosis Factor-α in Sera of Obese Patients: Fall with Weight Loss
Paresh Dandona,Ruth S. Weinstock,Kuldip Thusu,Ehad Abdel-Rahman,Ahmad Aljada,Thomas A. Wadden +5 more
Reads0
Chats0
TLDR
This study investigated whether serum TNFα concentrations are elevated in obese subjects, whether they fall after weight loss, and whether this fall parallels the fall in insulin release after glucose challenge.Abstract:
In view of the recent demonstration that obesity in animals and humans is associated with an increase in tumor necrosis factor-alpha (TNFalpha) expression, that this expression falls with weight loss, and that TNFalpha may specifically inhibit insulin action, the possibility that TNFalpha may be a mediator of insulin resistance has been raised. We have undertaken this study to investigate whether serum TNFalpha concentrations are elevated in obese subjects, whether they fall after weight loss, and whether this fall parallels the fall in insulin release after glucose challenge. Obese patients (age range: 25-54, weight mean +/- SD: 96.4 +/- 13.8 kg, body mass index: 35.7 +/- 5.6 kg/m2) were started on a diet program. The mean weight fell to 84.5 +/- 11.3 (P < 0.0001) and body mass index to 31.3 +/- 4.9 (P < 0.0001). Plasma TNFalpha concentrations were markedly elevated in the obese (3.45 +/- 0.16 pg/mL), when compared with controls (0.72 +/- 0.28 pg/mL), and fell significantly (2.63 +/- 1.40 pg/mL) after weight loss (P < 0.02). The magnitude of insulin release after glucose (75 g) challenge (area under the curve) also fell significantly (P < 0.01) after weight loss. The magnitude of weight loss and fall in TNFalpha were related to basal body weight (r = 0.57, P < 0.001) and basal TNFalpha (r = 0.55, P < 0.001) concentrations, respectively, but not to each other or to the glucose-induced insulin release (area under the curve). We conclude that obesity is associated with increased plasma TNFalpha concentrations, which fall with weight loss. Because circulating TNFalpha may mediate insulin resistance in the obese, a fall in TNFalpha concentrations may contribute to the restoration of insulin resistance after weight loss, Thus, TNFalpha may be an important circulating cytokine, which may provide a potentially reversible mechanism for mediating insulin resistance.read more
Citations
More filters
Journal ArticleDOI
Subcutaneous and visceral adipose tissue : Their relation to the metabolic syndrome
TL;DR: Methods for assessment of several phenotypes of human obesity, with special reference to abdominal fat content, have been evaluated and the endocrine regulation of abdominal visceral fat in comparison with the adipose tissue localized in other areas is presented.
Journal ArticleDOI
Inflammation: the link between insulin resistance, obesity and diabetes.
TL;DR: The increased concentrations of TNF-alpha and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction, which might interfering with the anti-inflammatory effect of insulin, which in turn might promote inflammation.
Journal ArticleDOI
Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance
TL;DR: Plasma IL-6 was significantly higher in obese subjects and demonstrated a highly significant inverse relationship with S(I) (r = -0.71, P < 0.001), while plasma TNF was significantly associated with plasma nonesterified fatty acid levels (r=0.49, P = 0.002).
Journal ArticleDOI
Obesity, inflammation, and insulin resistance.
TL;DR: The rapidly expanding body of animal and clinical data that support potential roles for inflammation in the pathogenesis of insulin resistance and type 2 diabetes mellitus are reviewed.
Journal ArticleDOI
CCR2 modulates inflammatory and metabolic effects of high-fat feeding
Stuart P. Weisberg,Deborah Hunter,Reid Huber,Jacob E. Lemieux,Sarah Slaymaker,Kris Vaddi,Israel F. Charo,Rudolph L. Leibel,Anthony W. Ferrante +8 more
TL;DR: The data suggest that CCR2 influences the development of obesity and associated adipose tissue inflammation and systemic insulin resistance and plays a role in the maintenance of adipOSE tissue macrophages and insulin resistance once obesity and its metabolic consequences are established.
References
More filters
Journal ArticleDOI
Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance
TL;DR: A role for TNF-alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity is indicated.
Journal ArticleDOI
Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance.
TL;DR: A role for the abnormal regulation of this cytokine in the pathogenesis of obesity-related insulin resistance is suggested as well as the effects of weight reduction by dietary treatment of obesity on the adipose expression of TNF-alpha mRNA.
Journal ArticleDOI
Changes in Energy Expenditure Resulting from Altered Body Weight
TL;DR: Maintenance of a reduced or elevated body weight is associated with compensatory changes in energy expenditure, which oppose the maintenance of a body weight that is different from the usual weight, which may account for the poor long-term efficacy of treatments for obesity.
Journal ArticleDOI
The expression of tumor necrosis factor in human adipose tissue. Regulation by obesity, weight loss, and relationship to lipoprotein lipase.
TL;DR: The data suggest that endogenous TNF expression in adipose tissue may help limit obesity in some subjects, perhaps by increasing insulin resistance and decreasing LPL.
Journal ArticleDOI
The Response to Long-Term Overfeeding in Identical Twins
Claude Bouchard,Angelo Tremblay,Jean-Pierre Després,André Nadeau,Paul J. Lupien,Germain Thériault,Jean H. Dussault,Sital Moorjani,Sylvie Pinault,G Fournier +9 more
TL;DR: It is concluded that the most likely explanation for the intrapair similarity in the adaptation to long-term overfeeding and for the variations in weight gain and fat distribution among the pairs of twins is that genetic factors are involved.