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The study investigated the effects of early life overfeeding on metabolic alterations, heart morphology and left ventricular insulin signaling pathway, mainly the glucose transporters GLUT1, GLUT4 and pAKT/AKT ratio. Wistar rats were overfed using the litter size reduction method. The pups were studies at age of 10 and 21 days. We measured heart GLUT1, GLUT4, AKT and pAKT. Animal weight and length, total body lipid, glycogen content, and the plasma levels of insulin, glucose, total cholesterol and triglycerides were measured. Cardiac hypertrophy was evaluated by heart weight/tibia length ratio. Our results showed that overfed animals were overweight, displayed high total body lipids, insulin, glucose, cholesterol and triglycerides plasma levels, and left ventricular hypertrophy with increasing of pAKT/AKT ratio. Moreover, the heart of overfed animals displayed a precocious translocation of GLUT4 and decreased content of GLUT1. In conclusion, we suggest that overfeeding during lactation might induce metabolic and cardiac alterations early in life, leading to the development of cardiac hypertrophy due anticipated insulin dependence created by earlier GLUT4 heart appearance. [ABSTRACT FROM AUTHOR]

Objective: Studies suggest the implication of CD16(+) subpopulations (CD14(+)CD16(+), CD14(dim)CD16(+)) in inflammatory diseases. We aimed to determine the frequency of these subpopulations during weight loss in obesity and diabetes, conditions associated with changes in systemic inflammation, and we tested the link with subclinical atherosclerosis., Methods and Results: CD14(dim)CD16(+) and CD14(+)CD16(+) frequencies were measured by flow cytometry in lean subjects, obese subjects before and after a hypocaloric diet or gastric surgery, and obese diabetic subjects before and after gastric surgery. Both monocyte subsets were increased in obese subjects, with a significant enrichment of the CD14(dim)CD16(+) subpopulation in obese diabetic patients. Multivariate analysis demonstrated a link between the percentages of CD14(dim)CD16(+) monocytes and glycemia, independent of fat mass. Drastic weight loss led to a sharp decrease of this subset, the variations of which were strongly related to fat mass changes. A reduction of at least 5% of fat mass was sufficient to observe a significant decrease of CD14(dim)CD16(+) monocytes. A diminution of the CD14(+)CD16(+) subset was also observed during weight loss and was associated with a decrease in intima-media thickness., Conclusions: This work demonstrates a major impact of fat mass variations on CD14(dim)CD16(+) monocyte subsets and that the decrease in the CD14(+)CD16(+) subpopulation is linked to a reduction of subclinical atherosclerosis., Clinical Trial Registration: URL: http://clinicaltrials.gov. Unique identifier: NCT00476658.