What question did this study set out to answer?

To determine the role of galectin-3 deficiency in high-fat diet-induced obesity, metabolic dysfunction, and inflammation in visceral fat and pancreatic islets.

January 25, 2013DiabetesOpen Access

Galectin-3 Deficiency Accelerates High-Fat Diet–Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets

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Authors

NPNada PejnovićUniversity of Belgrade JPJelena PantićUniversity of Vienna IJIvan JovanovićUniversity of Kragujevac

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Implication

Animal study reveals that galectin-3 ablation accelerates obesity and inflammation in mice on a high-fat diet, indicating a protective role against metabolic disease.

Key Points

To determine the role of galectin-3 deficiency in high-fat diet-induced obesity, metabolic dysfunction, and inflammation in visceral fat and pancreatic islets.
Fed wild-type and galectin-3-deficient (LGALS3-/-) mice a high-fat diet to evaluate obesity progression, insulin resistance, and tissue inflammation.
Profiled immune cell populations, advanced glycation end products (AGEs), and NLRP3 inflammasome components in visceral adipose tissue and pancreatic islets.
Stimulated isolated peritoneal macrophages in vitro with LPS and palmitate, assessing IL-1β production and NF-κB signaling alongside NLRP3 siRNA silencing.
High-fat diet-fed LGALS3-/- mice showed increased body weight, visceral adipose tissue mass, fasting blood glucose, insulin resistance, and systemic inflammatory markers compared with wild-type controls.
LGALS3-/- animals exhibited increased type 1 T/NKT cells, proinflammatory macrophages, AGE/RAGE expression, mature caspase-1, and phosphorylated NF-κB p65 in adipose and islet tissues, alongside decreased regulatory T cells.
In vitro stimulation of LGALS3-/- macrophages produced elevated caspase-1-dependent IL-1β and NF-κB phosphorylation, which was mitigated by NLRP3 siRNA knockdown.

Cite This Study

Pejnović et al. (2013) studied this question.

synapsesocial.com/papers/6a71f0df78a11c550e0bdf13 https://doi.org/10.2337/db12-0222

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Implication

Animal study reveals that galectin-3 ablation accelerates obesity and inflammation in mice on a high-fat diet, indicating a protective role against metabolic disease.

Galectin-3 Deficiency Accelerates High-Fat Diet–Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets

Discussion

Member takes

Implication

Key Points

Cite This Study

Galectin-3 Deficiency Accelerates High-Fat Diet–Induced Obesity and Amplifies Inflammation in Adipose Tissue and Pancreatic Islets

Discussion

Member takes

Implication

Key Points

Cite This Study

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