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Effect of Short-Term Hyperglycemia on Adipose Tissue Fluxes of Selected Cytokines In Vivo During Multiple Phases of Diet-Induced Weight Loss in Obese Women

Publikace na 3. lékařská fakulta |
2015

Tento text není v aktuálním jazyce dostupný. Zobrazuje se verze "en".Abstrakt

Context: Hyperglycemia is suggested to be one of the drivers of the proinflammatory state observed in obese and diabetic patients. Objectives: The objectives of the study was to investigate whether sc abdominal adipose tissue (scAT) could be one of the important sources of proinflammatory cytokines released in response to short-term hyperglycemia and whether this secretion capacity could be influenced by weight loss.

Design, Patients, and Interventions: Output of cytokines and proteins of acute phase from scAT in response to a 3-hours hyperglycemic clamp was evaluated in nine obese women in vivo using Fick's principle. Moreover, the output of cytokines was analyzed during a multiphase dietary intervention consisting of 1 month on a very low-calorie diet and subsequent 5-month weight-stabilization phase.

Main Outcome Measure(s): The levels of cytokines and proteins of acute phase [IL-6, IL-8, IL-1 receptor antagonist (IL-1Ra), TNF-alpha, monocyte chemoattractant protein-1 (MCP-1), serum amyloid A, and C-reactive protein] in arterial and venous plasma were measured during each dietary phase. The insulin sensitivity of scAT in respect to the antilipolytic effect of insulin during the clamp was assessed.

Results: Hyperglycemia increased the output of cytokines IL-6, MCP-1, and IL-1Ra from scAT. This effect had a tendency to be reduced after weight loss.

The output of other proinflammatory substances from scAT into circulation was not detected. The diet-induced weight loss was associated with the improvement of antilipolytic insulin sensitivity in scAT.

Conclusions: The results suggest that short-term hyperglycemia induces an increase of the output of cytokines IL-6, IL-1Ra, and MCP-1 from adipose tissue, and this deleterious hyperglycemia effect may be attenuated by the diet-induced weight reduction. This lowered responsiveness of the inflammation-related system may be an important feature of the weight reduction-induced improvement of the metabolic status of obese prediabetic individuals.