Postprandial lipid abnormalities in type 2 diabetes mellitus.

AIM AND OBJECTIVES: To study the postprandial lipid abnormalities in patients with type 2 diabetes mellitus. MATERIAL AND METHODS: Postprandial lipids were studied in 20 male type 2 diabetic subjects (age 49.75 +/- 4.82 years) and 20 age and sex matched healthy controls (age 49.55 +/- 4.82 years) after an oral fat challenge which consisted of a meal providing 729 keal/m2 body surface area with 68 gm fat. RESULTS: Average duration of diabetes among diabetic was 2.32 +/- 3.03 years. The body mass index (cases 25.84 +/- 4.52; controls 25.74 +/- 5.0; p > 0.05) and waist-hip ratio (cases 1.06 +/- 0.13; controls 1.14 +/- 0.2; p > 0.05) were similar in both groups. While fasting serum lipids were not significantly different between the two groups, a number of serum lipid abnormalities were noted in type 2 diabetic subjects in the postprandial state. These included a higher triglyceride-area under curve (AUC) (cases 1298.08 +/- 485.2 vs. controls 922.15 +/- 390.47 mg/dl/8h; p=0.01), a higher triglyceride-area under incremental curve (AUIC) (cases 549.68 +/- 382.24; control 294.75 +/- 172.6 mg/dl/8h; p=0.01), a higher peak triglyceride level (cases 425.2 +/- 204.47 mg%, controls 283.9 +/- 11.6.94 mg%, p=0.01), a lower HDL-AUC (cases 130.35 +/- 33.55 vs. controls 168.48 +/- 56.01 mg/dl/8h, p=0.013) and a lower HDL nadir (Cases 28.05 +/- 10.94 mg%, controls 37.13 +/- 13.52 mg%, p < 0.02). Triglyceride AUC correlated significantly with fasting serum triglyceride (r=0.62) and BMI (r=0.7), but not with waist hip ratio or fasting serum insulin levels. Postprandial lipaemia did not correlate with age, duration of diabetes, fasting blood glucose or glycosylated hemoglobin. CONCLUSION: In conclusion, make type 2 diabetics demonstrate significant postprandial lipid abnormalities, particularly of triglycerides, which appear to be independent of glycaemic control.

Autonomic neuropathy in patients with hepatic cirrhosis.

BACKGROUND: Autonomic neuropathy has been reported in patients with alcoholic liver disease but information on its occurrence in patients with non-alcoholic liver disease is contradictory. AIM: To assess autonomic functions in patients with alcoholic and non-alcoholic liver disease. STUDY DESIGN: Autonomic function using five standard tests was examined in 20 cirrhotics (10 alcoholics and 10 non-alcoholics) and 20 age and sex matched controls. The extent of autonomic dysfunction was determined in the patients and a comparison between the characteristics of patients with and without autonomic neuropathy was made. RESULTS: Sixteen (80%) of the cirrhotic subjects were found to have evidence of autonomic neuropathy. Of these, three (15%) patients had early parasympathetic damage, five (25%) had definite parasympathetic damage, and eight (40%) had combined (that is, both parasympathetic and sympathetic) damage. Nine (90%) of the alcoholics and seven (70%) of the non-alcoholics had autonomic dysfunction. Only one patient belonging to the alcoholic group had clinical evidence of peripheral neuropathy. Moreover, there was no significant association between subjective symptoms of autonomic neuropathy and objective evidence of autonomic damage as assessed by autonomic function tests. Autonomic dysfunction was significantly more frequent in advanced liver disease compared with early liver damage. Nine (75%) out of 12 cirrhotic subjects belonging to Child class B and six (85.7%) of the seven patients belonging to Child class C had autonomic neuropathy. CONCLUSION: This study shows that autonomic neuropathy is common in cirrhotic subjects, that it is found with comparable frequency in alcoholics and non-alcoholics, and that it increases in severity with increase in extent of liver damage, suggesting that liver damage contributes to the neurological deficit.