Molina A, Pita A, Farriol M, Virgili N, Soler J, Gómez J M
Department of Endocrinology and Nutrition, Ciutat Sanitària I Universitària de Bellvitge L'Hospitalet de Llobregat, Barcelona, Spain.
Clin Nutr. 2000 Oct;19(5):333-8. doi: 10.1054/clnu.2000.0110.
Short-bowel syndrome is a state of severe malabsorption resulting from absence or removal of the small bowel for several causes. A number of short-bowel patients develop hyperphagia. Leptin, a protein secreted from adipose tissue, signals the amount of energy stores to the brain.
To study body composition and leptin regulation in short-bowel patients and to determine whether or not leptin concentrations are linked with hyperphagia.
We studied 25 short-bowel patients (remnant bowel less than 150 cm) and 31 controls and 10 oral nutrition. Fifteen patients received total parenteral nutrition and 10 oral nutrition. Anthropometric measurements, body composition (by bioelectrical impedance), and cholesterol, triacylglycerol and leptin concentrations were studied in all subjects.
There were no differences between short-bowel patients and controls in anthropometric variables, body composition, or leptin concentrations. Leptin concentrations were higher in short-bowel women than men (9.21+/-8.54 vs. 3.22+/-1.86 ng/ml, P=0.01). Leptin concentrations correlated positively with age (r=0.4, P=0.045), body mass index (r=0.52, P=0.007), fat mass (r=0.67, P=0.001) and body fat (r=0.68, P=0.0001); there were no correlations with other body composition parameters. We found no correlations between parenteral or oral nutrition and body composition parameters, or between leptin concentrations and the presence of hyperphagia. Logistic regression analysis showed that body fat correctly identified leptin concentrations in 60% of patients.
Body composition, leptin concentrations and leptin regulation in patients with short-bowel syndrome are similar to those of controls. Leptin concentrations do not correlate with hyperphagia in short bowel-patients.
短肠综合征是由于多种原因导致小肠缺失或切除而引起的严重吸收不良状态。许多短肠患者会出现食欲亢进。瘦素是一种由脂肪组织分泌的蛋白质,它向大脑传递能量储存量的信号。
研究短肠患者的身体成分和瘦素调节情况,并确定瘦素浓度是否与食欲亢进有关。
我们研究了25名短肠患者(残余肠管小于150厘米)、31名对照者和10名接受口服营养的患者。15名患者接受全胃肠外营养,10名患者接受口服营养。对所有受试者进行人体测量、身体成分(通过生物电阻抗法)以及胆固醇、三酰甘油和瘦素浓度的研究。
短肠患者与对照者在人体测量变量、身体成分或瘦素浓度方面没有差异。短肠女性的瘦素浓度高于男性(9.21±8.54对3.22±1.86纳克/毫升,P = 0.01)。瘦素浓度与年龄呈正相关(r = 0.4,P = 0.045)、与体重指数呈正相关(r = 0.52,P = 0.007)、与脂肪量呈正相关(r = 0.67,P = 0.001)以及与体脂呈正相关(r = 0.68,P = 0.0001);与其他身体成分参数无相关性。我们发现胃肠外营养或口服营养与身体成分参数之间、瘦素浓度与食欲亢进的存在之间均无相关性。逻辑回归分析表明,体脂在60%的患者中能正确识别瘦素浓度。
短肠综合征患者的身体成分、瘦素浓度和瘦素调节与对照者相似。短肠患者的瘦素浓度与食欲亢进无关。