Correlation of insulin‑resistance with blood fat and glucose in elder patients after surgery for hepatic carcinoma

Abstract

The present study was designed to analyze variations in blood fat, blood glucose and insulin-resistance in elder patients following surgery for hepatic carcinoma. It also investigated the correlation of insulin with the level of serum leptin and blood fat. A total of 80 patients with primary hepatic cancer who were admitted to The First Hospital of Lanzhou University for treatment between October 2014 and June 2016 were enrolled in the study. At the 1-year follow-up, the patients were divided into two groups based on their recurrence of hepatic cancer after surgery. The levels of serum leptin were detected prior to, one month and one year after surgery; the changes in blood fat, body mass index (BMI), waistline and hipline were measured at one year after surgery; alterations in the fasting blood glucose and blood glucose were measured at 2 h after meal. The fasting insulin (FINS) level and homeostasis model assessment-insulin resistance (HOMA-IR) index were also measured. Correlations between serum leptin and total cholesterol, FINS and fasting blood glucose were analyzed. In the recurrence group, the levels of serum leptin and FINS level were significantly reduced, while waistline and hipline were increased, compared with the non-recurrence group (P<0.05). The BMI and fasting blood glucose in the recurrence group was significantly elevated in comparison with the non-recurrence group (P<0.05). The HOMA-IR index was significantly increased in the recurrence group compared with the non-recurrence group (P<0.05). These results indicated that following surgery for hepatic cancer, the level of serum leptin in patients with recurrence was decreased with an increase in susceptibility to abnormal metabolism of blood fat and glucose. In addition, the serum leptin was negatively correlated with the total cholesterol level and fasting blood glucose and positively correlated with the FINS level in patients. It was concluded that leptin levels decreased in patients with postoperative recurrence, as well as the accumulation of visceral adipose tissue and the development of abnormal blood glucose metabolism was observed.

Correlation analysis of obesity phenotypes with leptin and adiponectin

“…And BMI was independently correlated with LEP in obese subjects. Other studies also observed that LEP was positively correlated with BMI, FINS and Homa-IR 40 , 41 , suggesting that elevation in LEP in the MUO group is associated with glucose metabolism disorders attributable to high BMI values. LEP levels could increase with adipocyte gain and bind to the leptin receptor (LEP-R), leading to the inhibition of food intake and enhanced energy expenditure 42 .…”

Prediction of the incidence of colorectal cancer by routine laboratory tests and anthropometric measurements about metabolism

“…Obesity is concerned most in multitudinous factors. Excess body fatness causes cancer of digestive organs such as gastric cardia, liver, gallbladder, pancreas, colon and rectum [10][11][12], due to a variety of biological mechanisms such as microenvironmental in ammation and immune mediated responses, hyperinsulinemia, insulin resistance, oxidative stress and insulin-like growth factors [13][14][15]. Prospective cohort studies found that obese participants had a statistically increased risk of multiple cancer mortality [16][17][18].…”

Prediction of the incidence of colorectal cancer by routine laboratory tests and anthropometric measurements about metabolism

“…Obesity is concerned most in multitudinous factors. Excess body fatness causes cancer of digestive organs such as gastric cardia, liver, gallbladder, pancreas, colon and rectum [10][11][12], due to a variety of biological mechanisms such as microenvironmental in ammation and immune mediated responses, hyperinsulinemia, insulin resistance, oxidative stress and insulin-like growth factors [13][14][15]. Prospective cohort studies found that obese participants had a statistically increased risk of multiple cancer mortality [16][17][18].…”