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Objective: Catch-up growth, a risk factor for later type 2 diabetes, is characterized by hyperinsulinemia, accelerated body-fat recovery (catch-up fat), and enhanced glucose utilization in adipose tissue. Our objective was to characterize the determinants of enhanced glucose utilization in adipose tissue during catch-up fat.Research Design and Methods: White adipose tissue morphometry, lipogenic capacity, fatty acid composition, insulin signaling, in vivo glucose homeostasis, and insulinemic response to glucose were assessed in a rat model of semistarvation-refeeding. This model is characterized by glucose redistribution from skeletal muscle to adipose tissue during catch-up fat that results solely from suppressed thermogenesis (i.e., without hyperphagia).Results: Adipose tissue recovery during the dynamic phase of catch-up fat is accompanied by increased adipocyte number with smaller diameter, increased expression of genes for adipogenesis and de novo lipogenesis, increased fatty acid synthase activity, increased proportion of saturated fatty acids in triglyceride (storage) fraction but not in phospholipid (membrane) fraction, and no impairment in insulin signaling. Furthermore, it is shown that hyperinsulinemia and enhanced adipose tissue de novo lipogenesis occur concomitantly and are very early events in catch-up fat.Conclusions: These findings suggest that increased adipose tissue insulin stimulation and consequential increase in intracellular glucose flux play an important role in initiating catch-up fat. Once activated, the machinery for lipogenesis and adipogenesis contribute to sustain an increased insulin-stimulated glucose flux toward fat storage. Such adipose tissue plasticity could play an active role in the thrifty metabolism that underlies glucose redistribution from skeletal muscle to adipose tissue. [ABSTRACT FROM AUTHOR]

Objective:To evaluate the ontogeny of adipose tissue dynamics in obese and lean Zucker rat pups, from suckling to puberty.Methods:The trial had a two-group parallel design. Sixty-two male Zucker rat pups shared within 15 litters received deuterated water for 5 days, prior killing at different age. Adipose tissues were collected for 2H-enrichment analyses using mass spectrometry to determine fat cell proliferation and lipid synthesis rates. Rats were assigned to obese and lean rat groups by genotyping.Results:The time course (from days 13 to 55) of all adipose tissue growth showed that the highest fractional rates of fat cell proliferation, triacylglycerol (TG) synthesis and de novo lipogenesis (DNL) took place during early suckling in all rat pups. The appearance of excessive fat mass growth in the obese rats, as compared with lean rats, was first shown through a significant increase in DNL at the end of suckling (P<0.05). The TG synthesis rate was enhanced (P<0.05) from the end of suckling and early postweaning until day 55 (from 122±10 to 498±78 in obese pups and from 25±6 to 75±26 mg new TG per day in lean pups (median±s.e.m., P<0.01)). In contrast, only by day 55 did the fractional proliferation rate of fat cells in retroperitoneal and epididymal depots in the obese rats supersede that of the lean rats (P<0.05).Conclusion:The early suckling period constitutes the most active period for adipose tissue development in normal rats. In the obese Zucker rat model, adipose hypertrophy primarily contributes to the early onset of obesity, while hyperplasia increases after puberty.Early onset of adipose tissue growth may play a determinant role in the development of obesity later in life.International Journal of Obesity (2008) 32, 648–657; doi:10.1038/sj.ijo.0803787; published online 18 December 2007 [ABSTRACT FROM AUTHOR]

Background:The growing prevalence of childhood overweight and obesity has renewed interest in determining the influence of the maternal and infant diet on the risk of developing excess fat mass later in life.Approach:Review of available human and animal data reporting the effects of dietary fat and fat types early in life on adipose development.Results:Rodent studies tend to show that maternal high-fat feeding during pregnancy and lactation results in increased adiposity of the offspring. Nevertheless, today there is a lack of population-based studies investigating this potential detrimental effect of maternal high-fat intake. Most epidemiological studies, performed so far, do not find any association between the level of dietary fat intake of infants and children and body weight and/or fatness. Regarding fat types exposure to high levels of dietary n-6 fatty acids during gestation and post-natal life, has been shown to promote obesity in mice. Nevertheless, other rodent studies do not demonstrate such an effect.Conclusion:There is no evidence supporting a restriction of fat intake during the first two post-natal years but the potential detrimental effects of maternal high-fat intake during gestation should be further investigated. The role of dietary fat types as early determinants of childhood obesity has so far been poorly studied. Robust evidence to support the adipogenic effects of n-6 fatty acids enriched-diets is currently lacking but this hypothesis is of importance and should be further evaluated in different animal models as well as in longitudinal human studies.International Journal of Obesity (2006) 30, S50–S57. doi:10.1038/sj.ijo.0803519 [ABSTRACT FROM AUTHOR]

Phloretin is a flavonoid found exclusively in apples and in apple-derived products where it is present as the glucosidic form, namely, phloridzin (phloretin 2'-O-glucose). In the present study, we compared the changes in plasma and urine concentrations of these two compounds in rats fed a single meal containing 0.25% phloridzin or 0.157% phloretin (corresponding to the ingestion of 22 mg of phloretin equivalents). In plasma, phloretin was recovered mainly as the conjugated forms (glucuronided and/or sulfated) but some unconjugated phloretin was also detected. By contrast, no trace of intact phloridzin was detected in plasma of rats fed a phloridzin meal. These compounds presented different kinetics of absorption; phloretin appeared more rapidly in plasma when rats were fed the aglycone than when fed the glucoside. However, whatever compound was administered, no significant difference in the plasma concentrations of total phloretin were observed 10 h after food intake. At 24 h after the beginning of the meal, the plasma concentrations of phloretin were almost back to the baseline, indicating that this compound was excreted rapidly in urine. The total urinary excretion rate of phloretin was not affected by the forms administered, and was estimated to be 8.5 micromol/24 h in rats fed phloretin or phloridzin. Thus, 10.4% of the ingested dose was recovered in urine after 24 h. [ABSTRACT FROM AUTHOR]