Weight regain after sustained weight reduction is accompanied by suppressed oxidation of dietary fat and adipocyte hyperplasia

Abstract

A dual-tracer approach (dietary 14C-palmitate and intraperitoneal 3H-H2O) was used to assess the trafficking of dietary fat and net retention of carbon in triglyceride depots during the first 24 h of weight regain. Obesity-prone male Wistar rats were allowed to mature under obesogenic conditions for 16 wk. One group was switched to ad libitum feeding of a low-fat diet for 10 wk (Obese group). The remaining rats were switched to an energy-restricted, low-fat diet for 10 wk that reduced body weight by 14% and were then assessed in energy balance (Reduced group), with free access to the low-fat diet (Relapse-Day1 group), or with a provision that induced a minor imbalance (+10 kcal) equivalent to that observed in obese rats (Gap-Matched group). Fat oxidation remained at a high, steady rate throughout the day in Obese rats, but was suppressed in Reduced, Gap-Matched, and Relapse-Day1 rats though 9, 18, and 24 h, respectively. The same caloric excess in Obese and Gap-Matched rats led to less fat oxidation over the day and greater trafficking of dietary fat to visceral depots in the latter. In addition to trafficking nutrients to storage, Relapse-Day1 rats had more small, presumably new, adipocytes at the end of 24 h. Dietary fat oxidation at 24 h was related to the phosphorylation of skeletal muscle acetyl-CoA carboxylase and fatty acid availability. These observations provide evidence of adaptations in the oxidation and trafficking of dietary fat that extend beyond the energy imbalance, which facilitate rapid, efficient regain during the relapse to obesity.

Differential effects of high MUFA with high or low P/S ratio (polyunsaturated to saturated fatty acids) on improving hepatic lipolytic enzymes and mediating PPARγ related with lipoprotein lipase and hormone-sensitive lipase of white adipose tissue in diet-induced obese hamster

“…49 In streptozotocin-induced diabetic rats, high-fat diets with a high P/S ratio of 1.0 significantly improved glucose oxidation and incorporation into lipids in adipocyte tissue compared with low P/S ratio diets of 0.3. 10 Moreover, reducing body fat accumulation by lowering dietary fat amount was reported by Jackman et al 50 , who found that obese rats switched to ad libitum feedings of a low-fat diet resulted in a high, steady rate of fat oxidation compared with those switched to an energy-restricted and low-fat diet.…”

Intrinsic aerobic capacity impacts susceptibility to acute high-fat diet-induced hepatic steatosis

“…To assess dietary fatty acid oxidation, tissue retention and trafficking of dietary fat, and de novo lipogenesis, an in vivo, 24-h, dual-tracer study was performed as described previously (15,38). On day 2 of the 3-day HFD, animals received an intraperitoneal injection of 3 H2O (200 l, 1 mCi/ml) 1 h prior to the start of the dark cycle, which allows for tracer equilibration with total body water, and measurement of incorporation of tritium in extracted lipid serves as an estimate of net retention of carbon via de novo lipogenesis.…”

Regular exercise attenuates the metabolic drive to regain weight after long-term weight loss

“…The reductions in leptin and insulin (21,(23)(24)(25), in combination with a number of other neural, nutrient, and endocrine signals, convey an "energy deficit" signal to energy balance control centers within the brain. The result is an increased drive to eat (8,15,21,23,25) and a suppressed energy expenditure (9, 14, 25-27, 33, 35, 44). To maintain the reduced weight, food intake must be proactively limited to the level that expenditure is suppressed.…”

“…Peripherally, the increase in insulin sensitivity and reversal of metabolic inflexibility primes tissues to utilize and store the impending caloric excess in an energetically efficient manner, in part because the ability to regulate fat oxidation is restored (2,15,38,41). Additionally, studies in both humans and animals suggest that weight loss can lead to an increase in the number of adipocytes, which could facilitate the repletion and expansion of adipose tissue depots (15,24,25). Taken together, these observations provide evidence that the metabolic adaptations to weight reduction not only make it very difficult to sustain the necessary level of calorie restriction, but they also facilitate rapid, efficient weight regain when the inevitable bout of overfeeding occurs.…”