Genetic study for obesity patients and some biochemical parameters in Iraq

Obesity is a complex and escalating global health issue with significant implications for public health and individual well-being. This study looks into the genetic factors that make Iraqi patients fat. It focuses on the genes PPARG and ADRB (ADRB2 and ADRB3) and how they are connected to important biochemical factors. The study looks at how certain genetic polymorphisms affect different biochemical markers, such as lipid profiles, thyroid hormones (T3, T4, and TSH), fasting blood sugar, glycated hemoglobin (HbA1c) levels, and vitamin D3 levels. This study included a total of 100 obese patients and 50 healthy controls, matched for age and gender. We extracted and analyzed DNA using allele-specific real-time PCR to identify genetic polymorphisms. The results demonstrated statistically significant differences between patient and control groups in several biochemical markers. LDL cholesterol levels were significantly higher in patients (129.65 ± 3.25 mg/dL) compared to controls (86.64 ± 2.55 mg/dL), with a T-test value of 9.768 and a p-value of 0.0001. Similarly, triglyceride levels were elevated in patients (183.02 ± 4.62 mg/dL) compared to controls (122.73 ± 3.86 mg/dL), with a T-test value of 14.011 and a p-value of 0.0001. People with heterozygous mutations had significantly higher fasting blood sugar levels (220.86 ± 11.28 mg/dL) and homozygous mutations (246.67 ± 34.05 mg/dL) compared to people with the normal genotype (119.50 ± 8.39 mg/dL). This showed a high risk of glucose metabolism disorders (p-value = 0.0001). The analysis of genetic polymorphisms revealed that 44% of the patient group was heterozygous and 8% were homozygous for specific mutations, compared to 12% heterozygous and 0% homozygous in the control group (p < 0.01). Patients with these genetic variations exhibited significant alterations in lipid metabolism and thyroid function. Notably, T3 levels were higher in people with homozygous mutations (161.11 ± 19.97 ng/dL) compared to controls, and TSH levels were higher (4.32 ± 0.56 mIU/L) compared to people with normal genotypes, which suggests that these changes might have an effect on how metabolism works. This study provides valuable insights into the genetic and biochemical factors influencing obesity, highlighting the critical role of genetic variations in metabolic disturbances. The findings underscore the importance of incorporating genetic profiling into clinical management, paving the way for personalized therapeutic interventions to improve obesity prevention and treatment strategies.