Sajjad A, Mottershead M, Syn W K, Jones R, Smith S, Nwokolo C U
Department of Gastroenterology, University Hospital, Coventry, UK.
Aliment Pharmacol Ther. 2005 Aug 15;22(4):291-9. doi: 10.1111/j.1365-2036.2005.02562.x.
Insulin resistance and oxidative stress induced by products of small intestinal bacterial activity are putative factors in the pathogenesis of non-alcoholic steatohepatitis. Acylated ghrelin is the biologically active form of an orexigenic gastric hormone that modifies insulin sensitivity and body composition.
To investigate the effect of ciprofloxacin on small intestinal bacterial activity, ethanol, ghrelin and insulin in non-alcoholic steatohepatitis patients.
Twelve non-alcoholic steatohepatitis patients and 11 controls were studied before and after ciprofloxacin 500 mg b.d. for 5 days. After an overnight fast, 75 g glucose was ingested and blood was sampled every 20 min for 120 min. Acylated and total ghrelin, ethanol and insulin were measured. Small intestinal bacterial activity was detected by glucose hydrogen breath test.
Mean (range) integrated plasma acylated ghrelin which was 102 (21-241) and 202 (88-366) pg/mL . 2 h in non-alcoholic steatohepatitis and controls respectively (P = 0.015). This difference persisted after correction for body mass index and was unaffected by ciprofloxacin treatment. One of six non-alcoholic steatohepatitis patients positive for small intestinal bacterial activity remained positive after ciprofloxacin. In contrast, the one healthy control positive for small intestinal bacterial activity remained positive after ciprofloxacin (P = 0.025). Ethanol was detected in two subjects in each group, becoming immeasurable after ciprofloxacin. In non-alcoholic steatohepatitis patients median (range) fasting insulin increased from 113 (10-223) to 152 (32-396) pmol/L (P < 0.02), after ciprofloxacin. This was accompanied by similar changes in insulin resistance.
Small intestinal bacterial activity is common in non-alcoholic steatohepatitis. Low acylated ghrelin in non-alcoholic steatohepatitis cannot be attributed to small intestinal bacterial activity. Changes in fasting insulin and ethanol following ciprofloxacin suggest that these parameters may be influenced by small intestinal bacterial activity.
小肠细菌活动产物诱导的胰岛素抵抗和氧化应激是非酒精性脂肪性肝炎发病机制中的假定因素。酰化胃饥饿素是一种促食欲胃激素的生物活性形式，可改变胰岛素敏感性和身体组成。
研究环丙沙星对非酒精性脂肪性肝炎患者小肠细菌活动、乙醇、胃饥饿素和胰岛素的影响。
对12例非酒精性脂肪性肝炎患者和11例对照者在服用500毫克环丙沙星每日两次、共5天前后进行研究。过夜禁食后，摄入75克葡萄糖，每20分钟采集一次血样，共采集120分钟。检测酰化和总胃饥饿素、乙醇和胰岛素。通过葡萄糖氢呼气试验检测小肠细菌活动。
非酒精性脂肪性肝炎患者和对照者2小时时血浆酰化胃饥饿素的平均（范围）积分分别为102（21 - 241）和202（88 - 366）皮克/毫升（P = 0.015）。在校正体重指数后，这种差异仍然存在，且不受环丙沙星治疗的影响。6例小肠细菌活动呈阳性的非酒精性脂肪性肝炎患者中有1例在服用环丙沙星后仍为阳性。相比之下，1例小肠细菌活动呈阳性的健康对照者在服用环丙沙星后仍为阳性（P = 0.025）。每组各有2名受试者检测到乙醇，服用环丙沙星后变为无法检测到。在非酒精性脂肪性肝炎患者中，服用环丙沙星后空腹胰岛素中位数（范围）从113（10 - 223）皮摩尔/升增至152（32 - 396）皮摩尔/升（P < 0.02）。这伴随着胰岛素抵抗的类似变化。
小肠细菌活动在非酒精性脂肪性肝炎中很常见。非酒精性脂肪性肝炎中酰化胃饥饿素水平低不能归因于小肠细菌活动。环丙沙星治疗后空腹胰岛素和乙醇的变化表明，这些参数可能受小肠细菌活动影响。
