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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, RESULTS. Meshes: Adipose Tissue, Animals, Antibodies, Neutralizing, Blood Glucose, CD4-Positive T-Lymphocytes, CD40 Ligand, Disease Models, Animal, Fatty Liver, Inflammation Mediators, Insulin, Insulin Resistance, Lipid Metabolism, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Obesity, Panniculitis, Time Factors, Weight Gain.
user
Does cD40L deficiency ameliorate adipose tissue inflammation and metabolic manifestations of obesity in mice? Context: Obese adipose tissue shows hallmarks of chronic inflammation, which promotes the development of metabolic disorders. The mechanisms by which immune cells interact with each other or with metabolism-associated cell types, and the players involved, are still unclear. The CD40-CD40L costimulatory dyad plays a pivotal role in immune responses and in diseases such as atherosclerosis and may therefore be a mediator of obesity. Here we investigated whether CD40L is involved in adipose tissue inflammation and its associated metabolic changes. To assess a putative role of CD40L in obesity in vivo, we evaluated metabolic and inflammatory consequences of 18 weeks of high-fat feeding in CD40L(+/+) and CD40L(-/-) mice. In addition, C57Bl6 mice were injected with neutralizing anti-CD40L (αCD40L) antibody for 12 weeks while being fed a high-fat diet. Genetic deficiency of CD40L attenuated the development of diet-induced obesity, hepatic steatosis, and increased systemic insulin sensitivity. In adipose tissue, it impaired obesity-induced immune cell infiltration and the associated deterioration of glucose and lipid metabolism. Accordingly, αCD40L treatment improved systemic insulin sensitivity, glucose tolerance, and CD4(+) T-cell infiltration in adipose tissue with limited effects on adipose tissue weight.
assistant
CD40L plays a crucial role in the development of obesity-induced inflammation and metabolic complications. Final Decision: yes