BACKGROUND

The effects of low-calorie dieting in obesity are disappointing in the long run. The brain's energy homeostasis plays a key role in the regulation of body weight. We hypothesized that the cerebral energy status underlies an adaptation process upon body weight loss due to hypocaloric dieting in humans.

OBJECTIVE

We instructed 26 healthy obese participants to reduce body weight via replacement of meals by a commercial diet product for two weeks. The cerebral energy status was assessed by phosphorus magnetic resonance spectroscopy (31 PMRS) before and after low-caloric dieting as well as at follow-up. A standardized test buffet was quantified after body weight loss and at follow-up. Blood glucose metabolism and neurohormonal stress axis activity were monitored.

RESULTS

Weight loss induced a decline in blood concentrations of insulin ( = 0.002), C-peptide ( = 0.005), ACTH ( = 0.006), and norepinephrine ( = 0.012). ATP/Pi ( = 0.003) and PCr/Pi ratios ( = 0.012) were increased and NADH levels reduced ( = 0.041) after hypocaloric dieting. At follow-up, weight loss persisted ( < 0.001), while insulin, C-peptide, and ACTH increased ( < 0.005 for all) corresponding to baseline levels again. Despite repealed hormonal alterations, ratios of PCr/Pi remained higher ( = 0.039) and NADH levels lower ( = 0.007) 6 weeks after ending the diet. ATP/Pi ratios returned to baseline levels again ( = 0.168).

CONCLUSION

Low-calorie dieting reduces neurohormonal stress axis activity and increases the neuroenergetic status in obesity. This effect was of a transient nature in terms of stress hormonal measures. In contrast, PCr/Pi ratios remained increased after dieting and at follow-up while NADH levels were still reduced, which indicates a persistently unsettled neuroenergetic homeostasis upon diet-induced rapid body weight loss.