Increased Autophagy and Apoptosis in the Kidneys of Intrauterine Growth Restricted Rats.

BACKGROUND: IUGR has been associated with nephron loss and chronic kidney disease (CKD). MATERIALS AND METHODS: We examined autophagy and apoptosis markers in the kidneys of IUGR Sprague Dawley rats induced by maternal low protein diet (LP), comparing them to controls. The autophagy marker LC3B, the pro-apoptotic protein Bax, and the anti-apoptotic protein Bcl-2 were determined by quantitative immunoblotting. Immunohistochemical expressions of LC3B, Bax, and Bcl-2 were evaluated at 4 weeks age. Glomerular counts (by maceration techniques) were performed at 5 weeks. RESULTS: The LP diet offspring were lighter (P < 0.05). In IUGR kidneys, LC3B and Bax were increased at birth (p < 0.05, p < 0.001) and at 4 weeks (p < 0.0142, p < 0.0001), Bcl-2 was decreased at birth (p < 0.05), and there were less glomeruli (p < 0.01) at 5 weeks. CONCLUSIONS: Autophagy and apoptosis may have a role in IUGR associated decreased nephron number in Sprague rats.

Examination of carnitine palmitoyltransferase 1 abundance in white adipose tissue: implications in obesity research.

Carnitine palmitoyltransferase 1 (CPT1) is essential for the transport of long-chain fatty acids into the mitochondria for oxidation. Recently, it was reported that decreased CPT1b mRNA in adipose tissue was a contributing factor for obesity in rats. We therefore closely examined the expression level of Cpt1 in adipose tissue from mice, rats, and humans. Cpt1a is the predominate isoform in adipose tissue from all three species. Rat white adipose tissue has a moderate amount of Cpt1b mRNA, but it is very minor compared with Cpt1b expression in muscle. Total CPT1 activity in adipose tissue is also minor relative to other tissues. Both Cpt1a and Cpt1b mRNA were increased in gonadal fat but not inguinal fat by diet-induced obesity in mice. We also measured CPT1a and CPT1b expression in subcutaneous adipose tissue from human subjects with a wide range of body mass indexes (BMIs). Interestingly, CPT1a expression positively correlated with BMI (R = 0.46), but there was no correlation with CPT1b (R = 0.04). Our findings indicate that white adipose tissue fatty acid oxidation capacity is minor compared with that of metabolically active tissues. Furthermore, given the already low abundance of Cpt1b in white adipose tissue, it is unlikely that decreases in its expression can quantitatively decrease whole body energy expenditure enough to contribute to an obese phenotype.