Giannini E, Botta F, Cataldi A, Tenconi G L, Ceppa P, Barreca T, Testa R
Cattedra di Gastroenterologia, Universita di Genova, Italia.
Hepatogastroenterology. 1999 Jul-Aug;46(28):2422-5.
BACKGROUND/AIMS: Leptin is a peptide which regulates food intake and energy expenditure. Moreover, it is involved in the homeostasis of body composition and is linked to the regulation of insulin signaling, thus playing an important role in liver fat storage. Steatosis is a common finding in chronic hepatitis C, and both viral and metabolic factors have been suggested to explain the presence of this histological characteristic. In order to study leptin in chronic liver disease characterized by the presence of steatosis, we evaluated its serum levels in patients with nonalcoholic steatohepatitis (NASH), in chronic hepatitis C (CHC) patients with no histological findings of steatosis, and CHC patients with steatosis but no risk factors for its development.
We studied 6 male patients with NASH whose diagnosis was made on the basis of histological findings and clinical criteria. From among a cohort of 170 CHC patients we put together 2 groups of 6 male patients each (with or without steatosis at liver biopsy examination), who had no risk factors for NASH. Male patients were chosen in order to avoid gender influence on leptin levels. Further criteria for admission were similar impairment of liver metabolic function as assessed by the monoethylglycinexylidide (MEGX) test and, in patients with CHC, similar body mass index (BMI) and histological staging. Moreover, we evaluated leptin/BMI ratio, in order to rule out BMI influence on leptin levels. Leptin levels were assessed by means of radioimmunoassay.
We found that BMI was higher in NASH compared to CHC (27.2 +/- 2.9 vs. 23.9 +/- 1.8; p = 0.01). Analysis of serum leptin levels showed an increasing trend starting from patients with CHC without steatosis (3.2 +/- 0.4 ng/ml), through CHC patients with steatosis (4.2 +/- 0.7 ng/ml) up to patients with NASH (5.7 +/- 2 ng/ml), although the differences observed were not statistically significant. Moreover, the ratio of leptin to BMI also followed the same trend showing increasing values (CHC without steatosis = 0.04 +/- 0.02; CHC patients with steatosis = 0.17 +/- 0.03; NASH = 0.203 +/- 0.07). Leptin levels and BMI showed a significant relationship (n = 18; r = 0.60; p < 0.01).
The increasing trend observed in leptin serum levels among the different groups of patients showed that in chronic liver disease characterized by the presence of steatosis, leptin signaling is preserved. Moreover, CHC factors different from the metabolic ones should be investigated in order to explain the presence of steatosis. Further studies on broader groups of patients are needed to verify these preliminary results.
背景/目的：瘦素是一种调节食物摄入和能量消耗的肽。此外，它参与身体成分的稳态，并与胰岛素信号调节有关，因此在肝脏脂肪储存中起重要作用。脂肪变性是慢性丙型肝炎中的常见表现，病毒和代谢因素均被认为可解释这种组织学特征的存在。为了研究存在脂肪变性的慢性肝病中的瘦素，我们评估了非酒精性脂肪性肝炎（NASH）患者、无脂肪变性组织学表现的慢性丙型肝炎（CHC）患者以及有脂肪变性但无其发生风险因素的CHC患者的血清瘦素水平。
我们研究了6例根据组织学表现和临床标准确诊为NASH的男性患者。从170例CHC患者队列中，我们将其分为两组，每组6例男性患者（肝活检检查时有或无脂肪变性），这些患者无NASH风险因素。选择男性患者是为了避免性别对瘦素水平的影响。进一步的入选标准是通过单乙基甘氨酰二甲苯胺（MEGX）试验评估的肝脏代谢功能有相似损害，对于CHC患者，还有相似的体重指数（BMI）和组织学分期。此外，我们评估了瘦素/BMI比值，以排除BMI对瘦素水平的影响。通过放射免疫测定法评估瘦素水平。
我们发现NASH患者的BMI高于CHC患者（27.2±2.9 vs. 23.9±1.8；p = 0.01）。血清瘦素水平分析显示，从无脂肪变性的CHC患者（3.2±0.4 ng/ml）开始，到有脂肪变性的CHC患者（4.2±0.7 ng/ml），再到NASH患者（5.7±2 ng/ml），呈现出上升趋势，尽管观察到的差异无统计学意义。此外，瘦素与BMI的比值也呈现相同趋势，数值增加（无脂肪变性的CHC患者 = 0.04±0.02；有脂肪变性的CHC患者 = 0.17±0.03；NASH患者 = 0.203±0.07）。瘦素水平与BMI显示出显著相关性（n = 18；r = 0.60；p < 0.01）。
在不同组患者中观察到血清瘦素水平的上升趋势表明，在以脂肪变性为特征的慢性肝病中，瘦素信号传导得以保留。此外，应研究不同于代谢因素的CHC因素，以解释脂肪变性的存在。需要对更广泛的患者群体进行进一步研究以验证这些初步结果。
