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A single exercise session can affect appetite-regulating hormones and suppress appetite. The effects of short, regular physical activity breaks across the day on appetite are unclear. This study investigated the effects of breaking up sitting with high-intensity physical activity vs a single bout of moderate-intensity exercise and prolonged sitting on appetite control. In this randomised crossover trial, 14 sedentary, inactive adults (7 women) completed 3, 8-h experimental conditions: (i) prolonged sitting (SIT); (ii) 30 min of moderate-intensity exercise followed by prolonged sitting (EX-SIT), and (iii) sitting with 2 min 32 s of high-intensity physical activity every hour (SIT-ACT). Physical activity energy expenditure was matched between EX-SIT and SIT-ACT. Subjective appetite was measured every 30 min with acylated ghrelin and total peptide-YY (PYY) measured hourly in response to two standardised test meals. An ad libitum buffet meal was provided at the end of each condition. Based on linear mixed model analysis, total area under the curve for satisfaction was 16% higher (P = 0.021) and overall appetite was 11% lower during SIT-ACT vs EX-SIT (P = 0.018), with no differences between SIT-ACT and SIT. Time series analysis indicated that SIT-ACT reduced subjective appetite during the majority of the post-lunch period compared with SIT and EX-SIT, with some of these effects reversed earlier in the afternoon (P < 0.05). Total PYY and acylated ghrelin did not differ between conditions. Relative energy intake was 760 kJ lower during SIT-ACT vs SIT (P = 0.024). High-intensity physical activity breaks may be effective in acutely suppressing appetite; yet, appetite-regulating hormones may not explain such responses.

Adrenal insufficiency is a life-threatening condition requiring chronic glucocorticoid replacement therapy, as well as stress adaptation to prevent adrenal crises. To increase patients’ self-sustainability, education on how to tackle an adrenal crisis is crucial. All patients should carry the European Emergency Card.

Autoimmune Addison’s disease (AAD) is defined as primary adrenal insufficiency due to immune-mediated destruction of the adrenal cortex. This destruction of steroid-producing cells has historically been thought of as an irreversible process, with linear progression from an ACTH-driven compensated phase to overt adrenal insufficiency requiring lifelong glucocorticoid replacement. However, a growing body of evidence suggests that this process may be more heterogeneous than previously thought, with potential for complete or partial recovery of glucocorticoid secretion. Although patients with persistent mineralocorticoid deficiency despite preserved or recovered glucocorticoid function are anecdotally mentioned, few well-documented cases have been reported to date. We present three patients in the United Kingdom who further challenge the long-standing hypothesis that AAD is a progressive, irreversible disease process. We describe one patient with a 4-year history of mineralocorticoid-only Addison’s disease, a patient with spontaneous recovery of adrenal function and one patient with clinical features of adrenal insufficiency despite significant residual cortisol function. All three patients show varying degrees of mineralocorticoid deficiency, suggesting that recovery of zona fasciculata function in the adrenal cortex may occur independently to that of the zona glomerulosa. We outline the current evidence for heterogeneity in the natural history of AAD and discuss possible mechanisms for the recovery of adrenal function.

Childhood cancer survivors are at risk for developing endocrine disorders, including deficits in growth hormone, thyroid hormone and sex hormones. The influence these hormones have on cell growth and metabolism has raised concerns regarding the safety of their use as treatments in survivors of childhood cancer and brain tumors. This article offers a summary of current knowledge, controversies and areas for future research pertaining to this area.

The nutritional environment during development periods induces metabolic programming, leading to metabolic disorders and detrimental influences on human reproductive health. This study aimed to determine the long-term adverse effect of intrauterine malnutrition on the reproductive center kisspeptin-neurokinin B-dynorphin A (KNDy) neurons in the hypothalamic arcuate nucleus (ARC) of female offspring. Twelve pregnant rats were divided into ad-lib-fed (control, n  = 6) and 50% undernutrition (UN, n  = 6) groups. The UN group was restricted to 50% daily food intake of the control dams from gestation day 9 until term delivery. Differences between the two groups in terms of various maternal parameters, including body weight (BW), pregnancy duration, and litter size, as well as birth weight, puberty onset, estrous cyclicity, pulsatile luteinizing hormone (LH) secretion, and hypothalamic gene expression of offspring, were determined. Female offspring of UN dams exhibited low BW from birth to 3 weeks, whereas UN offspring showed signs of precocious puberty; hypothalamic Tac3 (a neurokinin B gene) expression was increased in prepubertal UN offspring, and the BW at the virginal opening was lower in UN offspring than that in the control group. Interestingly, the UN offspring showed significant decreases in the number of KNDy gene-expressing cells after 29 weeks of age, but the number of ARC kisspeptin-immunoreactive cells, pulsatile LH secretions, and estrous cyclicity were comparable between the groups. In conclusion, intrauterine undernutrition induced various changes in KNDy gene expression depending on the life stage. Thus, intrauterine undernutrition affected hypothalamic developmental programming in female rats.