Background: Obesity has become a significant global health issue. This multifaceted condition is influenced by genetic, environmental, and lifestyle factors, significantly influenced by nutrition. Aim: The study’s objective is to elucidate the relationship between obesity-related genes, nutrient intake, and the development of obesity and the importance of other metabolic diseases. Methods: A comprehensive literature review spanning the past two decades was conducted to analyze the contributions of genetic variants—including FTO, MC4R, and LEPR—and their associations with dietary habits, highlighting how specific nutrients affect gene expression and obesity risk and how the coexistence of metabolic diseases such as type 2 diabetes and osteoporosis may modulate these factors. Moreover, the role of epigenetic factors, such as dietary patterns that encourage the development of obesity, was explored. Discussion and Conclusions: By understanding the intricate relationships among genetics, nutrients, and obesity development, this study highlights the importance of personalized dietary strategies in managing obesity. Overall, an integrated approach that considers genetic predispositions alongside environmental influences is essential for developing effective prevention and treatment methodologies, ultimately contributing to better health outcomes in diverse populations.

Apolipoprotein M (apoM) is a 26-kDa protein expressed mainly in the liver and kidneys. It is present predominantly in high-density lipoproteins (HDL). ApoM expression is influenced by the hepatocyte nuclear factor-1alpha (HNF-1alpha), which is a transcription factor associated with the pathogenesis of MODY. Some earlier data suggested that apoM levels were lower in the serum of HNF-1alpha MODY subjects, than in that of other diabetics and healthy controls. The aim of this study was to evaluate apoM as a biomarker for HNF-1alpha MODY. We included in this study 48 HNF-1alpha mutation carriers (40 diabetic patients and 8 subjects with normal glucose levels in the fasted state) from the Polish Nationwide Registry of MODY. In addition, we examined 55 T2DM patients and 55 apparently healthy volunteers who had normal fasting glucose levels. ApoM was measured by the sandwich dot-blot technique with recombinant apoM (Abnova) as a protein standard, mouse anti-human apoM monoclonal primary antibody and rat anti-mouse HRP-conjugated secondary antibody (BD Biosciences). Mean apoM level in the MODY group was 13.6 mug/ml, SD 1.9 (13.5 mug/ml, SD 1.7 in diabetic subjects and 13.9 mug/ml, SD 2.0 in non-diabetic mutation carriers respectively). In the T2DM group, mean apoM level was 13.7 mug/ml, SD 2.1, while it reached 13.8 mug/ml, SD 2.0 in healthy controls. There was no difference between apoM serum concentrations in all the study groups. In summary, our study showed no association between HNF-1alpha mutations resulting in MODY phenotype and apoM levels. Thus, we cannot confirm the clinical usefulness of apoM as a biomarker of HNF-1alpha MODY.

OBJECTIVE—1,5-anhydroglucitol (1,5-AG) is a short-term marker of metabolic control in diabetes. Its renal loss is stimulated in hyperglycemic conditions by glycosuria, which results in a lowered plasma concentration. As a low renal threshold for glucose has been described in hepatocyte nuclear factor-1α (HNF-1α) maturity-onset diabetes of the young (MODY), the 1,5-AG level may be altered in these patients. The purpose of this study was to assess the 1,5-AG levels in patients with HNF-1α MODY and in type 2 diabetic subjects with a similar degree of metabolic control. In addition, we aimed to evaluate this particle as a biomarker for HNF-1α MODY. RESEARCH DESIGN AND METHODS—We included 33 diabetic patients from the Polish Nationwide Registry of MODY. In addition, we examined 43 type 2 diabetic patients and 47 nondiabetic control subjects. The 1,5-AG concentration was measured with an enzymatic assay (GlycoMark). Receiver operating characteristic (ROC) curve analysis was used to evaluate 1,5-AG as a screening marker for HNF-1α MODY. RESULTS—The mean 1,5-AG plasma concentration in diabetic HNF-1α mutation carriers was 5.9 μg/ml, and it was lower than that in type 2 diabetic patients (11.0 μg/ml, P = 0.003) and in nondiabetic control subjects (23.9 μg/ml, P < 0.00005). The ROC curve analysis revealed 85.7% sensitivity and 80.0% specificity of 1,5-AG in screening for HNF-1α MODY at the criterion of <6.5 μg/ml in patients with an A1C level between 6.5 and 9.0%. CONCLUSIONS—1,5-AG may be a useful biomarker for differential diagnosis of patients with HNF-1α MODY with a specific range of A1C, although this requires further investigation. However, the clinical use of this particle in diabetic HNF-1α mutation carriers for metabolic control has substantial limitations.

The cholesteryl ester transfer protein (CETP) gene encodes a hydrophobic glycoprotein that plays a crucial role in the reverse transport of cholesterol. The aim of the present study was to determine whether CETP polymorphisms (rs1532624, rs247616 and rs708272) are associated with coronary artery disease (CAD) in a Polish population. Serum lipid levels and single nucleotide polymorphisms of CETP genes were determined in 494 subjects: 248 patients with premature CAD and 246 blood donors as controls. Selected polymorphisms were examined using TaqMan PCR analysis. We found that CAD risk was significantly higher for CC homozygotes and C allele carriers of the rs247616 polymorphism than for carriers with the T allele (OR 1.89, 95% CI 1.29–2.76, p = 0.001 and OR 1.51, 95% CI 1.14–1.99, p = 0.003) and likewise for the CC genotype of the rs1532624 polymorphism than for those with the A allele (OR 1.59, 95% CI 1.05–2.40, p = 0.026). Moreover, T allele carriers of the rs708272 polymorphism had significantly higher total cholesterol levels compared to CC homozygotes (p < 0.05) in the healthy controls. We also observed an allelic pattern, C_(rs2477616)C_(rs708272)C_(rs1532624), which increased susceptibility to CAD by 43% (OR = 1.43, 95% CI 1.10–1.85, p = 0.006). In conclusion, the rs247616 and rs1532624 polymorphisms of CETP may modulate the risk of CAD in Polish population.

Reactive oxygen species (ROS) are involved in the pathogenesis of atherosclerosis and coronary artery disease (CAD). NADPH oxidases are the main source of ROS in the vasculature. p22phox is a critical component of vascular NADPH oxidases and is encoded by the CYBA (cytochrome b₂₄₅ alpha) gene. The −930A>G CYBA polymorphism (rs9932581:A>G) modulates the activity of the CYBA promoter, and influences CYBA transcriptional activity. The aim of the present study was to analyze a possible association between the −930A>G polymorphism and CAD and to search for gene–traditional risk factors interactions. 480 subjects were studied: 240 patients with premature CAD, 240 age and sex matched blood donors. The −930A>G polymorphism was genotyped using the TaqMan^® Pre-designed SNP Genotyping Assay (Applied Biosystems). The −930G allele carrier state was a risk factor for CAD (OR 2.03, 95 % CI 1.21–3.44, P = 0.007). A synergistic effect of the −930G allele with overweight/obesity (BMI ≥ 25) and cigarette smoking was found. The estimated CAD risk for BMI ≥ 25 and the −930G allele interaction was about 160 % greater than that predicted by assuming additivity of the effects, and about 40 % greater for interaction of cigarette smoking and the −930G allele. Overweight/obesity was a risk factor for CAD only in the −930G allele carriers (P < 10⁻¹⁰) but not in the AA homozygotes (P = 1.00). In conclusion the −930A>G CYBA polymorphism is associated with CAD in the Polish population. The −930G allele carriers are particularly at risk of consequences of obesity and tobacco smoke exposure.