Lipid Accumulation Product Index, Caspase-1 and Inflammatory Status of Diabetics in Port Harcourt, Nigeria

Abstract

Background: This study evaluated Lipid Accumulation Product (LAP) index, Caspase-1, and the Inflammatory Status of Diabetics in Port Harcourt, Nigeria. Materials and Methods: 165 subjects comprising 90 diabetic (test) subjects and 75 non-diabetic (control) subjects were recruited for the study. Fasting blood samples were collected for biochemical analyses. Fasting blood sugar (FBS) was determined using the enzymatic oxidation method. Glycated haemoglobin (HbA1c) was determined using the fluorescence immunoassay method. Caspase-1, tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and fasting insulin were determined using the enzyme-linked immunosorbent assay (ELISA) method. Insulin resistance was determined using the homeostatic model assessment of insulin resistance (HOMA-IR) method. Albumin (ALB) was determined using the bromocresol green (BCG) dye-binding method. Triglyceride (TG) was determined by enzymatic method. Lipid accumulation product index (LAPI) was calculated with the formula: [WC (cm) – 65] × [TG (mmol/L)] for men, and [WC (cm) – 58] × [TG (mmol/L)] for women. Results: HbA1c, FBS, and HOMA-IR were significantly higher (P<0.05) in diabetic subjects compared to the non-diabetic controls. There was no significant difference (P>0.05) in insulin levels in the diabetics and controls. LAPI, caspase-1, and IL-1β were significantly higher (P<0.05) in diabetic subjects compared to the controls. TNF-α showed no significant difference (P>0.05), while ALB levels were significantly lower (P<0.05) in diabetics compared to the controls. There were no significant differences (P>0.05) in LAPI, caspase-1, TNF-α, IL-1β and ALB levels in the diabetic subjects with varying years of illness, as caspase-1, TNF-α, and IL-1β remained elevated, while ALB levels remained reduced throughout the duration of diabetes. Correlation analysis showed LAPI was positively/significantly (P<0.05) correlated with HOMA-IR and IL-1β. HOMA-IR was significantly (P<0.05) and positively correlated with TNF-α. There was a significant (P<0.05) and positive correlation between Caspase-1 and TNF-α, and Caspase-1 and IL-1β. Albumin was negatively correlated with TNF-α and IL-1β. Conclusion: Type 2 diabetes is a chronic inflammatory disease characterised by hyperglycaemia, insulin resistance and lipid accumulation. Lifestyle and pharmacological interventions are recommended to abate the self-perpetuating cycle of inflammation, lipid accumulation, and metabolic dysfunction in diabetes.