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 31 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 (p = 0.002), C-peptide (p = 0.005), ACTH (p = 0.006), and norepinephrine (p = 0.012). ATP/Pi (p = 0.003) and PCr/Pi ratios (p = 0.012) were increased and NADH levels reduced (p = 0.041) after hypocaloric dieting. At follow-up, weight loss persisted (p < 0.001), while insulin, C-peptide, and ACTH increased (p < 0.005 for all) corresponding to baseline levels again. Despite repealed hormonal alterations, ratios of PCr/Pi remained higher (p = 0.039) and NADH levels lower (p = 0.007) 6 weeks after ending the diet. ATP/Pi ratios returned to baseline levels again (p = 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.
Keywords: 31 phosphorus magnetic resonance spectroscopy; adenosine triphosphate; body weight; brain; humans; hypocaloric dieting; obesity; phosphocreatine.