Abstract
BackgroundThe contribution of insulin to acne is that it stimulates the synthesis of androgenic hormones, which are important in the development of excess sebum, hyperkeratinization, and sebaceous gland cell growth. ObjectiveTo ascertain whether the lipid profile abnomalies seen in acne vulgaris are genetically induced, we also seek to establish a link between insulin resistance and lipid profiles. MethodsAn analytical cross-sectional study with case-control design research investigation of 72 individuals with acne vulgaris and 72 healthy volunteers was carried out. Both groups' medical histories were taken, as were the severity and duration of the disease among acne sufferers, as well as demographic data. Anthropometry tests were performed on both groups, including their weights, height, and circumference of waist, as well as the profile of lipids, blood glucose levels after a fast, insulin levels during fasting, resistance to insulin, and Apo B-48 folding change. ResultsSevere acne vulgaris patients showed significantly increased TG, TC, LDL-C, blood glucose levels after a fast, fasting insulin, and resistance to insulin levels. P = 0.005 showed that Apo B-48 expression increased in patients compared to healthy people. Apo B-48 folding change and insulin resistance were found to have a substantial positive simple linear association. Acne vulgaris, whether mild, moderate, or severe, has a significant positive linear connection with insulin resistance. ConclusionAcne patients had an abnormal in lipid profile. Acne individuals with severe form are more inclined to acquire resistance to insulin as well as higher glucose and insulin levels. Apo B-48 gene expression is elevated in acne individuals with severe form who have lipid abnormalities. This illustrating the importance of genetic variables in acne, insulin resistance, lipid profile modifications as well as Isotretinoin, a standard acne medication, can also cause lipid irregularities.
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