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Abstract
Background: Caloric restriction is a valid strategy to reduce the visceral adipose tissue (VAT) content in obese persons. Hypocretin-1 (orexin-A) is a neuropeptide synthesized in the lateral hypothalamus that strongly modulates food intake, thus influencing adipose tissue accumulation. Therapeutic diets in obesity treatment may combine the advantages of caloric restriction and dietary ketosis. The current study aimed to evaluate the effect of a very low calorie ketogenic diet (VLCKD) in a population of obese patients. Methods: Adiposity parameters and orexin-A serum profiling were quantified over an 8 week period. The effect of the VLCKD on reactive oxygen species (ROS) production and cell viability was evaluated, in vitro, by culturing Hep-G2 cells in the presence of VLCKD sera. Results: Dietary intervention induced significant effects on body weight, adiposity, and blood chemistry parameters. Moreover, a selective reduction in VAT was measured by dual-energy X-ray absorptiometry. Orexin-A levels significantly increased after dietary treatment. Hep-G2 cell viability was not affected after 24, 48, and 72 h incubation with patients’ sera, before and after the VLCKD. In the same model system, ROS production was not significantly influenced by dietary treatment. Conclusion: The VLCKD exerts a positive effect on VAT decrease, ameliorating adiposity and blood chemistry parameters. Furthermore, short-term mild dietary ketosis does not appear to have a cytotoxic effect, nor does it represent a factor capable of increasing oxidative stress. Finally, to the best of our knowledge, this is the first study that shows an effect of the VLCKD upon the orexinergic system, supporting the usefulness of such a therapeutic intervention in promoting obesity reduction in the individual burden of this disease.
Highlights
Obesity is a long-term multifactorial chronic disease characterized by an energy imbalance due to an excess of caloric intake compared with energy expenditure and the deregulation of other metabolic parameters, such as altered lipid profile, increased insulin resistance, and chronic proinflammatory state [1]
The aim of the present study was to quantify the effects of a commercial weight-loss dietary ketosis program on visceral fat mass, evaluated by dual-energy X-ray absorptiometry (DXA), and the impact of 8 weeks of treatment on orexin-A production and reactive oxygen metabolite (d-ROM) levels in vivo, in a population of obese patients treated with the very low calorie ketogenic diet (VLCKD), and in vitro, in Hep-G2 cells, to evaluate cell viability and oxidative stress in response to treatment with VLCKD sera before and after the weight-loss dietary ketosis program
Participants were excluded if they had a prior medical history of renal insufficiency, hyperuricemia, severe hepatic insufficiency, type 1 or 2 diabetes mellitus treated with insulin, atrioventricular block, heart failure, cardiovascular and cerebrovascular diseases, unbalanced hypokalemia, hypo- or hyperthyroidism, chronic treatment with corticosteroid drugs, severe mental disorders, neoplasms, pregnancy, or they were lactating
Summary
Obesity is a long-term multifactorial chronic disease characterized by an energy imbalance due to an excess of caloric intake compared with energy expenditure and the deregulation of other metabolic parameters, such as altered lipid profile, increased insulin resistance, and chronic proinflammatory state [1]. Obesity types may be distinguished between central (adipose tissue around the abdomen rather than appendicular accumulation) and visceral. The severity of obesity-related diseases is closely linked to visceral adiposity, considering that VAT may cause a subclinical systemic inflammation condition [3]. Obesity is characterized by an imbalance in the neurochemical pathways, orexin-A/hypocretin-1. Caloric restriction is a valid strategy to reduce the visceral adipose tissue (VAT) content in obese persons. Hypocretin-1 (orexin-A) is a neuropeptide synthesized in the lateral hypothalamus that strongly modulates food intake, influencing adipose tissue accumulation. The effect of the VLCKD on reactive oxygen species (ROS)
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