Zhang Yong, Li Fenxia, Liu Fu-Qiang, Chu Chao, Wang Yang, Wang Dan, Guo Tong-Shuai, Wang Jun-Kui, Guan Gong-Chang, Ren Ke-Yu, Mu Jian-Jun
Cardiovascular Department, Shaanxi Provincial People's Hospital, Xi'an 710068, China.
Cardiovascular Department, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710061, China.
Nutrients. 2016 May 26;8(6):323. doi: 10.3390/nu8060323.
Overweight/obesity is a chronic disease that carries an increased risk of hypertension, diabetes mellitus, and premature death. Several epidemiological studies have demonstrated a clear relationship between salt intake and obesity, but the pathophysiologic mechanisms remain unknown. We hypothesized that ghrelin, which regulates appetite, food intake, and fat deposition, becomes elevated when one consumes a high-salt diet, contributing to the progression of obesity. We, therefore, investigated fasting ghrelin concentrations during a high-salt diet. Thirty-eight non-obese and normotensive subjects (aged 25 to 50 years) were selected from a rural community in Northern China. They were sequentially maintained on a normal diet for three days at baseline, a low-salt diet for seven days (3 g/day, NaCl), then a high-salt diet for seven days (18 g/day). The concentration of plasma ghrelin was measured using an immunoenzyme method (ELISA). High-salt intake significantly increased fasting ghrelin levels, which were higher during the high-salt diet (320.7 ± 30.6 pg/mL) than during the low-salt diet (172.9 ± 8.9 pg/mL). The comparison of ghrelin levels between the different salt diets was statistically-significantly different (p < 0.01). A positive correlation between 24-h urinary sodium excretion and fasting ghrelin levels was demonstrated. Our data indicate that a high-salt diet elevates fasting ghrelin in healthy human subjects, which may be a novel underlying mechanism of obesity.
超重/肥胖是一种慢性疾病,会增加患高血压、糖尿病和过早死亡的风险。多项流行病学研究已证明盐摄入量与肥胖之间存在明确关联,但其病理生理机制仍不清楚。我们推测,调节食欲、食物摄入量和脂肪沉积的胃饥饿素,在人们食用高盐饮食时会升高,从而导致肥胖的进展。因此,我们研究了高盐饮食期间的空腹胃饥饿素浓度。从中国北方的一个农村社区选取了38名非肥胖且血压正常的受试者(年龄在25至50岁之间)。他们在基线时先连续三天保持正常饮食,然后进行七天的低盐饮食(3克/天,氯化钠),接着进行七天的高盐饮食(18克/天)。采用免疫酶法(ELISA)测量血浆胃饥饿素浓度。高盐摄入显著提高了空腹胃饥饿素水平,高盐饮食期间(320.7±30.6皮克/毫升)的水平高于低盐饮食期间(172.9±8.9皮克/毫升)。不同盐饮食之间胃饥饿素水平的比较具有统计学显著差异(p<0.01)。24小时尿钠排泄量与空腹胃饥饿素水平之间呈正相关。我们的数据表明,高盐饮食会提高健康人体受试者的空腹胃饥饿素水平,这可能是肥胖的一种新的潜在机制。