Key result
Intravenous LPS administration increased adipose tissue expression of LPL, HSL, and adiponectin in control subjects but not in patients with T2DM (interaction p=0.03, p=0.02, and p=0.02).
Why the study?
Does adipose tissue in patients with T2DM display an altered metabolic and inflammatory response to systemic LPS administration compared to controls?
Does adipose tissue in patients with T2DM display an altered metabolic and inflammatory response to systemic LPS administration compared to controls?
p-value: p=0.03, p=0.02, p=0.02
Patients with T2DM demonstrate an altered, resistant adipose tissue response to systemic LPS regarding mediators of lipolysis and lipogenesis, which may contribute to inflammation-related metabolic complications.
T2DM adipose tissue shows blunted lipolytic/adiponectin responses to LPS despite similar cytokine induction; leaves open its role in diabetic metabolic dysfunction.
Aim: Inflammation is thought to play a major role in impaired metabolism.However, the metabolic and inflammatory response of adipose tissue, to a pro-inflammatory stimulus is poorly defined in patients with Type 2 Diabetes Mellitus (T2DM).We therefore aimed to investigate whether adipose tissue in T2DM would display an altered response to E. coli LipoPolySaccharide (LPS). Materials and methods:Twelve patients with T2DM and 12 control subjects received an intravenous bolus injection of LPS (0.3 ng/kg).Abdominal subcutaneous adipose tissue biopsies, serum and plasma were obtained at 0, 2, 4, 6 and 8 hours after LPS.The gene expression of Tumour Necrosis Factor-α (TNF), InterLeukin-6 (IL-6), lipoprotein lipase (LPL), hormone sensitive lipase (HSL), fatty acid synthase (FASN), adiponectin and peroxisome proliferator-activated recptor γ (PPARγ) was analysed by real time reverse transcription Polymerase Chain Reaction (PCR).Results: The expression of TNF and IL-6 in adipose tissue increased after LPS administration without any difference between groups (2-way ANOVA, effect of time: p<0.001 and p=0.0001, respectively).In contrast, the expression of LPL, HSL and adiponectin in adipose tissue increased only in control subjects (2-way ANOVA, effect of time X group: p=0.03; p=0.02 and p=0.02, respectively).There was no effect of LPS on FASN or PPARγ in either group.Conclusion: Patients with T2DM demonstrate a resistance to LPS in terms of inducing important mediators of lipolysis and lipogenesis, although the expression of TNF and IL-6 in adipose tissue increased in both groups.And thus, adipose tissue may contribute to the acute inflammation-related metabolic complications seen in T2DM.
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Neha Mathur (2012) studied Type 2 Diabetes Mellitus (n=24). E. coli LipoPolySaccharide (LPS) vs. Control subjects was evaluated on Gene expression of LPL, HSL, and adiponectin in adipose tissue (p=p=0.03, p=0.02, p=0.02). Intravenous LPS administration increased adipose tissue expression of LPL, HSL, and adiponectin in control subjects but not in patients with T2DM (interaction p=0.03, p=0.02, and p=0.02).
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