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Adipocyte Hypertrophy and Improved Postprandial Lipid Response in Beta 2 Syntrophin Deficient Mice.

BACKGROUND/AIMS
Adipocyte hypertrophy in obesity is associated with inflammation and adipose tissue fibrosis which both contribute to metabolic diseases. Mechanisms regulating lipid droplet expansion are poorly understood. Knock down of the scaffold protein beta 2 syntrophin (SNTB2) increases lipid droplet size of 3T3-L1 adipocytes and the physiological relevance of SNTB2 in adipose tissue morphology and metabolic health was analyzed herein.


METHODS
Wild type and SNTB2-/- mice were challenged with 24 weeks high fat diet. Adipose tissue morphology and expression of various genes / proteins including collagens and caveolin-1 was examined. Glucose, insulin, fasting and fed free fatty acids were measured in serum. SNTB2 expression was determined in adipose tissues of patients.


RESULTS
Upon high fat diet SNTB2-/- mice displayed reduced adiposity and adipocyte hypertrophy. Expression of various proteins was normal in the different white fat depots of SNTB2-/- mice while caveolin-1 protein and collagen mRNA levels were diminished. Null mice had reduced systemic glucose while fasting and postprandial insulin and insulin response were normal. Fatty acid clearance in the fed state and after insulin injection was enhanced. SNTB2 and caveolin-1 were increased in fat of ob/ob mice. However, no correlation between body mass index and SNTB2 protein in adipose tissues of seven patients was found. In subcutaneous but not in visceral fat the ratio of SNTB2 to alpha syntrophin protein, which affects lipid droplet size in the opposite manner, was associated with BMI. In subcutaneous fat of extremely obese patients SNTB2 mRNA levels were not correlated with weight loss after bariatric surgery.


CONCLUSION
Current study shows that high SNTB2 in obese adipose tissues restricts adipocyte growth and thereby may contribute to metabolic diseases.