Insulin resistance and liver fibrosis progression in patients with chronic hepatitis C virus infection

Hepatitis C virus [HCV] infection can predispose to development of insulin resistance before diabetes occurs. Such a potential link is particularly cogent in light of recent date indicating that diabetes might be associated with increased hepatic fibrosis progression in patients with chronic HCB infection. This study aims to determine the prevalence of insulin resistance in non-diabetic patients with chronic hepatitis C and its relation to liver fibrosis. This study included a cohort of 38 patients with chronic liver diseases. They were subdivided into two groups: chronic hepatitis C [CHC] with elevated liver enzymes and CHC with normal liver enzymes. Twelve age- and sex-matched healthy subjects were considered as the control group. The cohort was subjected to careful history and complete examination stressing upon the signs and symptoms of chronic liver diseases. Investigations include liver function test, viral markers [anti-HCV antibodies and polymerase chain reaction [PCR] for HCV], serum fasting glucose, serum fasting insulin and homeostasis model assessment [HOMA], liver biopsy and abdominal ultrasound. Liver fibrosis was found to be considerably more severe among HCV patients elevated serum transaminases levels. No correlation between viral load and hepatic fibrosis in HCB-infected patients was found. Insulin resistance was present in HCV-infected cases compared with the control group and it correlated with liver fibrosis positively. The present data support the hypothesis that insulin resistance may increase the rate of fibrosis progression in non-diabetic patients with chronic HCV. Follow-up of hyperinsulinaemia by serial measurements of HOMA test in non-diabetic HCV-infected patients may be a biochemical indicator for progression of liver fibrosis

Aging is an inevitable risk factor for insulin resistance

The present work looks into the different aspects of glucose homeostasis in the elderly patients in comparison to healthy younger subjects and patients with type 2 diabetes mellitus, relying on intravenous glucose tolerance test. A clinicobiochemical study was carried out comprising forty apparently healthy non-diabetic non-obese old individuals [mean age 65 +/- 4.8 years]. Forty type 2 diabetic patients compared to thirty healthy young subjects. The senile group had no family history of diabetes. Cases with renal, hepatic, gastrointestinal, or endocrine abnormalities were excluded from the study. Intravenous glucose tolerance test [ivGTT] was done with sampling at 0, 5, 10, 15, 30, 45, and 60 min after glucose load and the following estimations were undertaken: glucose constant decay [KG], glucose and insulin area under the curve, insulnogenic index, first phase insulin response, insulin resistance index and fractional insulin clearance. The senile and diabetic groups, when compared to the control, had non-significantly different fasting plasma glucose in senile group but it was higher in diabetic patients, while fasting serum insulin was significantly higher in the studied groups than in healthy control group. The senile group showed significant reduction in glucose tolerance [KG 1.36 +/- 0.3%/min], decreased insulin sensitivity index [5.19 +/- 1.4 10[-4] min[-1] /[uIU/ml]] and marked reduction of first phase insulin response [2.45 +/- 0.78 uIU/ml per mg/dl], when compared with the control group. However, the degree of glucose intolerance and insulin insensitivity of the senile group was still significantly less than of type 2 diabetic patients. This study revealed that the insulin resistance seems to be characteristic feature of normal aging process and senility could be considered as an inevitable risk factor for glucose intolerance and metabolic syndrome with its accompanying health hazards. Insulin secretion, insulin clearance and interaction between insulin and target tissues are defective in elderly subjects. These functions are intermediate between healthy controls and type 2 diabetic patients and may predispose the elderly population to the risk of impaired glucose tolerance or diabetes mellitus with its attendant macrovascular and microvascular complications