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Why lost weight returns after dieting

Published on June 30, 2004 at 8:39 PM · No Comments

After months of torturous dieting, there is nothing more frustrating than to find that the lost weight has returned. Many dieters are shocked to see they have returned to their original weight despite modifications in exercise and eating habits. Now a new animal study reveals that when loss occurs, metabolic adaptations occur that mandate a return of the undesired pounds.

These findings address a key question of whether regaining loss weight due to dieting is caused by metabolic or behavioral changes. The common belief is that the metabolic state after weight loss promotes weight regain. However, data germane to this supposition has been controversial and equivocal.

The failure to reach definitive conclusions in between these studies is linked to the way metabolic mass is estimated, the selection of research subjects, and the methods of weight loss and weight maintenance. Human studies are impractical, because there is no way to identify individuals predisposed to the development of obesity. Even if such identification was possible, it would be difficult to follow them throughout the protracted course of the development, treatment, and recurrence of their obese state.

Rats offer a better opportunity to address this issue. The ability to select obesity-prone rats, coupled with the shorter lifespan of the test animals and a better ability to control environmental conditions, offers researchers the opportunity to examine the metabolic state of an obese rat.

This is the framework of a study performed through an assessment of indirect calorimetry, the balance of energy and fuel utilization in these obesity-prone rats throughout five stages of obesity development, treatment, and recurrence. Those stages are (1) pre-obesity; (2) established obesity; (3) weight-reduced; (4) weight-reduced after a period of weight maintenance; and (5) weight-reduced after a period of regaining the lost weight.

The goal of the study was to collect data that offered insight to the metabolic adjustments that occur in response to weight loss and maintenance that make successful weight maintenance a challenging prospect.

The authors of the study, “Metabolic Adjustments with the Development, Treatment, and Recurrence of Obesity in Obesity-Prone Rats,” are Paul S. MacLean, Janine A. Higgins, Ginger C. Johnson, Brooke K. Fleming-Elder, and James O. Hill, from the University of Colorado Health Sciences Center, Denver, CO; and John C. Peters, from the Procter and Gamble Company. Their findings appear in the online edition of the American Journal of Physiology – Regulatory, Integrative and Comparative Physiology. The journal is one of 14 published each month by the American Physiological Society (www.the-aps.org).

The study design consisted of placing 13 obesity-prone rats on a high fat diet for a period of 16 weeks to promote the development of obesity. These obese rats were examined metabolically and represent a group of rats with established obesity (established obesity, EO). These rats were then placed on a low fat, energy restricted diet that would produce a 10-15 percent loss in body weight during two weeks of caloric restriction and again underwent metabolic examination (weight loss, WL). Weight loss was targeted to achieve a 10-15 percent loss in body weight that would be reflective of target adjustments in human weight loss programs. To achieve this objective, weight loss was induced by limiting calories to approximately 60 percent of energy expenditure, with a daily monitoring and adjustment of food intake throughout the 14-day period to ensure a negative energy balance.

Six of the 13 calorically restricted rats were then assigned to a weight maintained group (WM), while the other seven were randomly assigned to a weight regain group (WR). The assignment of the rats to WM and WR groups was based upon having the two groups stratified by body weight and total weight loss. WM rats were subsequently maintained at this reduced weight with restricted energy intake for eight weeks before again being examined, while WR rats were allowed to regain weight with at-will access to a low fat diet for eight weeks before being examined. Three other separate groups were employed as controls. One group of seven rats was examined immediately after the screening process (pre-obesity, PO). Another group of seven rats was fed a high fat diet for 16 weeks and then examined after being switched to a low fat diet for 10 weeks to represent an age-matched diet-matched control (low fat diet control, LFC). The last group of eight rats was fed a high fat diet for 16 weeks, as with the other groups, but examined after being continued with this regimen for another 10 weeks (high fat diet control, HFC). Body weight was monitored regularly throughout the entire study. Energy balance, fuel utilization and body composition were determined at specified time points corresponding to the various stages of the development, treatment, and recurrence of obesity.

The goal of the research was to determine if there is a metabolic propensity to regain weight after a period of significant weight loss. Accordingly, 24 hour energy expenditure (EE), sleeping metabolic rate (SMR), and non-protein respiratory quotient (NPRQ) were obtained by indirect calorimetry with urinary nitrogen analysis and normalized to fat mass (FM) and fat free mass (FFM) acquired by dual energy x-ray absorptiometry.

This study provides insight as to how the metabolic state of an obesity-prone rat changes from the pre-obese state to the obese state.

The first conclusion reached from the data is that the transition from the pre-obese to the obese state is accompanied by an increase in metabolic rate and metabolic efficiency but little alteration in the utilization of fuels outside of that explained by the variation in the type and amount of diet consumed.

The obesity-prone rats in the present study do reflect obesity-prone humans in a number of aspects. Accordingly, when compared to obesity-resistant counterparts, obesity-prone rats: (1) eat more; (2) have a lower 24-hr energy expenditure under conditions leading to obesity ; and (3) have an elevated 24 hour NPRQ on both low and high fat diets.

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