Korbonits Márta, Blaine David, Elia Marinos, Powell-Tuck Jeremy
Department of Endocrinology, Barts and the London Medical School, UK.
Eur J Endocrinol. 2007 Aug;157(2):157-66. doi: 10.1530/EJE-06-0740.
The discovery of leptin, a hormone primarily involved in adaptation to fasting, led to an increased interest in appetite regulation and appetite-modulating hormones. Here, we present unique data from a case of extreme starvation and refeeding, showing changes in plasma concentrations of appetite-modulating and metabolic hormones as well as biochemical changes, and draw attention to the dangers of the refeeding syndrome.
We studied the refeeding period of a 44-day voluntary fast uncomplicated by underlying disease. Biochemical and hormonal variables were compared with 16 matched subjects such that the BMI range of the controls covered the entire spectrum for the index subject's recovering BMI.
Lack of calorie intake with free access to water resulted in 25% loss of body weight. Haemoconcentration was observed and feeding was started with a low sodium, hypocaloric liquid formulation. During early refeeding, marked hypophosphataemia, haemodilution and slight oedema developed. Vitamins B1, B12 and B6 were depleted while serum free fatty acids, ketone bodies and zinc levels were abnormally high; abnormal liver function developed over the first week. The hormonal profile showed low IGF-I and insulin levels, and elevated IGF-binding protein-1 concentrations. Appetite-regulating hormones were either very low (leptin and ghrelin) or showed no marked difference from the control group (peptide YY, agouti-related peptide, alpha-melanocyte-stimulating hormone, neuropeptide Y and pro-opiomelanocortin). Appetite was low at the beginning of refeeding and a transient increase in orexin and resistin was observed coincidently with an increase in subjective hunger.
Our study illustrates the potential dangers of refeeding and provides a comprehensive insight into the endocrinology of prolonged fasting and the refeeding process.
瘦素是一种主要参与禁食适应过程的激素，其发现引发了人们对食欲调节及食欲调节激素的更多关注。在此，我们展示了一例极度饥饿与再喂养病例的独特数据，呈现了食欲调节激素和代谢激素的血浆浓度变化以及生化改变，并提请注意再喂养综合征的危险性。
我们研究了一名44天自愿禁食且无基础疾病并发症患者的再喂养期。将生化和激素变量与16名匹配受试者进行比较，以使对照组的体重指数（BMI）范围涵盖指数受试者恢复过程中BMI的整个范围。
在可自由饮水但缺乏热量摄入的情况下，体重减轻了25%。观察到血液浓缩，开始采用低钠、低热量液体配方进行喂养。在早期再喂养期间，出现了明显的低磷血症、血液稀释和轻度水肿。维生素B1、B12和B6耗竭，而血清游离脂肪酸、酮体和锌水平异常升高；第一周内出现肝功能异常。激素水平显示胰岛素样生长因子-I（IGF-I）和胰岛素水平较低，而IGF结合蛋白-1浓度升高。食欲调节激素要么非常低（瘦素和胃饥饿素），要么与对照组无明显差异（肽YY、刺鼠相关肽、α-黑素细胞刺激素、神经肽Y和阿片促黑素皮质素原）。再喂养开始时食欲较低，同时观察到食欲肽和抵抗素短暂升高，主观饥饿感也随之增加。
我们的研究阐明了再喂养的潜在危险性，并对长期禁食及再喂养过程中的内分泌学提供了全面的见解。
