Body composition and hormonal responses to a carbohydrate-restricted diet

doi:10.1053/meta.2002.32037

Metabolism

Volume 51, Issue 7, July 2002, Pages 864-870

https://doi.org/10.1053/meta.2002.32037 Get rights and content

Abstract

The few studies that have examined body composition after a carbohydrate-restricted diet have reported enhanced fat loss and preservation of lean body mass in obese individuals. The role of hormones in mediating this response is unclear. We examined the effects of a 6-week carbohydrate-restricted diet on total and regional body composition and the relationships with fasting hormone concentrations. Twelve healthy normal-weight men switched from their habitual diet (48% carbohydrate) to a carbohydrate-restricted diet (8% carbohydrate) for 6 weeks and 8 men served as controls, consuming their normal diet. Subjects were encouraged to consume adequate dietary energy to maintain body mass during the intervention. Total and regional body composition and fasting blood samples were assessed at weeks 0, 3, and 6 of the experimental period. Fat mass was significantly (P [le ] .05) decreased ([minus ]3.4 kg) and lean body mass significantly increased (+1.1 kg) at week 6. There was a significant decrease in serum insulin ([minus ]34%), and an increase in total thyroxine (T₄) (+11%) and the free T₄ index (+13%). Approximately 70% of the variability in fat loss on the carbohydrate-restricted diet was accounted for by the decrease in serum insulin concentrations. There were no significant changes in glucagon, total or free testosterone, sex hormone binding globulin (SHBG), insulin-like growth factor-I (IGF-I), cortisol, or triiodothyronine (T₃) uptake, nor were there significant changes in body composition or hormones in the control group. Thus, we conclude that a carbohydrate-restricted diet resulted in a significant reduction in fat mass and a concomitant increase in lean body mass in normal-weight men, which may be partially mediated by the reduction in circulating insulin concentrations.

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Mean R-BHB_fast increased significantly during KD + PL (1.0 mM BHB), an effect enhanced 26% during KD + KS. GLU_fast AUC was −6% lower during KD + KS versus LFD. Mean R-BHB_diur increased 40% in KD + KS versus KD + PL, whereas GLU_diur decreased 13% during both KDs versus LFD. R-BHB_KS peaked (Δ: ∼1 mM) 1 h after the morning KS dose, but not following the afternoon dose. Both R/S-BHB_plasma increased during KD independent of KS inclusion. R-BHB_plasma was 50-times greater compared to S-BHB_plasma, and the KS augmented S-BHB_plasma 50% more than PL. Fasting insulin and HOMA-IR decreased after 14 days independent of diet.
A hypocaloric KD was effective at reducing diurnal glucose compared to a LFD independent of weight loss, but twice-daily racemic KS ingestion during KD augmented ketonemia, both as R- and S-BHB, and decreased mean fasting glucose beyond a KD alone. The hypoglycemic effects of KD in combination with exogenous ketones merit further investigation.
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Polycystic ovaries (PCO) is a hormonal disorder that is a leading cause of infertility. The formation of multiple persistent cysts and hormonal imbalance are hallmarks of PCO. Recent clinical studies reported a beneficial effect of the ketogenic diet (KD; high-fat, low-carbohydrate) on PCO. The aim of this study was to investigate the effect of the KD alone and in combination with metformin on letrozole-induced PCO in female rats.
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Ketogenic diet with sustained hyper-ketonemia above 1 mol/l has the same impact as low carbohydrate non-ketogenic diet on muscle strength, body-composition, and hormonal and lipid profile in hypo-caloric dietary conditions in strength-trained middle-aged men.
Sex-specific effects of ketogenic diet after pre-exposure to a high-fat, high-sugar diet in rats
2021, Nutrition, Metabolism and Cardiovascular Diseases
Citation Excerpt :
Although our work focused on the overall changes after dietary intervention, more work needs to be done to understand the behavioral and endocrine changes that occur when individuals start different types of dietary interventions. KDs have shown to alter energy expenditure in men and ketones have been shown to increase lipolysis differently in women than in men [10,41,42]. One potential link that is being explored between the relationships in therapeutic effects of KD, is the mediating role of peroxisome proliferator-activated receptors (PPARs).
The objectives were to evaluate the relationship between ketogenic diets, the ketone body beta-hydroxybutyrate (BHB), parameters known to increase risk for cardiovascular and metabolic diseases in both sexes, using a pre-clinical model of obesity.
Rats had access to a diet high in fat and sugar (HFS) for 12 weeks. After HFS, they switched to chow (HFS–CH) or ketogenic diet (HFS-KD) for 3 weeks to model a dietary intervention. Body weight, adiposity, and food intake were measured. Glucose tolerance and corticosterone response to stress were measured after HFS, then again after the intervention. Both sexes increased body weight, food intake, and adiposity compared to control (CTL) while on HFS. HFS females showed impaired glucose tolerance. HFS males developed a dampened corticosterone to stress, whereas HFS females developed an exacerbated response. The effects of HFS on adiposity and corticosterone were reversed in HFS–CH males. These same improvements were observed in HFS–CH females, although they still had impaired glucose tolerance. HFS-KD males showed some improvements, however, they still had higher body weight and adiposity than CTL. The same pattern was observed in females. These beneficial effects of KD correlated with plasma BHB levels in females but not in males.
These data model effects reported in clinical literature and serve as a valuable translational tool to further test causal mechanisms that lead to desirable outcomes of KD. These sex-specific relationships are important, as KD could potentially affect endocrine mechanisms differently in males and females.

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^☆: Supported by a grant from the Atkins Foundation, New York, NY.

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Body composition and hormonal responses to a carbohydrate-restricted diet☆

Abstract