Fasting for 48 h induced similar glucose intolerance in both sexes despite greater perceived stress and decreased estradiol levels in females.

PURPOSE: The purpose of this study was to compare the effects of fasting for 48 h on the evoked insulin and glucose responses in males and females, and to explore factors such as stress and estrogen levels that might influence these responses. METHODS: Healthy, nonobese male (n = 14) and female (n = 14) subjects underwent 48-h fasting trial. Changes in glucose tolerance and insulin levels in response to the oral glucose tolerance test, subjectively perceived stress and catecholamine concentrations were measured in all participants. Estrogen levels were also measured in the female participants during the 48-h fast. RESULTS: Glucose area under the curve (AUC) values increased similarly in both sexes after 48-h fasting (P < 0.05), but females displayed a greater rise in insulin AUC values than males (P < 0.05). Fasting increased plasma epinephrine concentrations in both sexes (P < 0.05), whereas plasma norepinephrine concentrations and subjective stress increased only in females (P < 0.05). Plasma 17-ß-estradiol concentrations in females decreased after fasting (P < 0.05). CONCLUSION: Fasting for 48 h induced a similar glucose intolerance in females and males, despite decreased 17-ß-estradiol levels and greater psychological and physiological stress in females. These differences represent a plausible explanation for the gender-based differences observed in insulin responses. TRIAL REGISTRATION: Retrospectively registered on ClinicalTrials.gov (NCT05545943) in September 19, 2022.

Short-duration cold exposure decreases fasting-induced glucose intolerance but has no effect on resting energy expenditure.

The aim of the present study was to investigate whether brief cold exposure can reverse fasting-induced glucose intolerance and insulin resistance, and improve resting energy expenditure (REE). Twelve young non-obese women were randomly assigned to undergo the following conditions: 2 days of fasting with two 10-min whole-body cold-water immersions on separate days (FAST-COLD), 2 days of fasting without cold-water immersions (FAST), 2 days of usual diet with two 10-min whole-body cold-water immersions on separate days (COLD), or 2 days of usual diet without cold-water immersions (CON) in a randomised crossover fashion. Changes in REE and substrate utilisation, and glucose tolerance and insulin sensitivity from the oral glucose tolerance test were examined. The results showed that FAST-COLD and FAST trials increased (P < 0.05) REE and decreased (P < 0.05) respiratory quotient, but these variables did not differ significantly between the FAST-COLD and FAST trials. The glucose and insulin area under the curves (AUCs) were higher (P < 0.05) in the FAST-COLD and FAST trials than in the CON and COLD trials, and these AUCs were lower (P < 0.05) in the FAST-COLD than in the FAST trial. Matsuda index was lower in the FAST trial than in the CON trial (P < 0.05), and tended to be greater after the FAST-COLD trial than after the FAST trial (P = 0.060). In conclusion, cold exposure had no effect on REE but decreased fasting-induced glucose intolerance which was accompanied by a maintained insulin sensitivity.

Prolonged fasting outperforms short-term fasting in terms of glucose tolerance and insulin release: a randomised controlled trial.

Fasting is related to glucose intolerance and insulin resistance, but it is unknown whether the duration of fasting influences these factors. We explored whether prolonged fasting increases norepinephrine and ketone concentrations and decreases core temperature to a greater extent than short-term fasting; if so, this should lead to improved glucose tolerance. Forty-three healthy young adult males were randomly assigned to undergo a 2-d fast, 6-d fast or the usual diet. Changes in rectal temperature (TR), ketone and catecholamine concentrations, glucose tolerance and insulin release in response to an oral glucose tolerance test were assessed. Both fasting trials increased ketone concentration, and the effect was larger after the 6-d fast (P < 0·05). TR and epinephrine concentration increased only after the 2-d fast (P < 0·05). Both fasting trials increased the glucose area under the curve (AUC) (P < 0·05), but the AUC remained higher than the baseline value after participants returned to their usual diet in the 2-d fast group (P < 0·05). Neither fasting had an immediate effect on the insulin AUC, although it increased after return to their usual diet in the 6-d fast group (P < 0·05). These data suggest that the 2-d fast elicited residual impaired glucose tolerance, which may be linked to greater perceived stress during short-term fasting, as shown by the epinephrine response and change in core temperature. By contrast, prolonged fasting seemed to evoke an adaptive residual mechanism that is related to improved insulin release and maintained glucose tolerance.