Insulin is a critical hormone that promotes energy storage in various tissues, as well as anabolic functions. Insulin resistance significantly reduces these responses, resulting in pathological conditions, such as obesity and type 2 diabetes mellitus (T2DM). The management of insulin resistance requires better knowledge of its pathophysiological mechanisms to prevent secondary complications, such as cardiovascular diseases (CVDs). Recent evidence regarding the etiological mechanisms behind insulin resistance emphasizes the role of energy imbalance and neurohormonal dysregulation, both of which are closely regulated by autophagy. Autophagy is a conserved process that maintains homeostasis in cells. Accordingly, autophagy abnormalities have been linked to a variety of metabolic disorders, including insulin resistance, T2DM, obesity, and CVDs. Thus, there may be a link between autophagy and insulin resistance. Therefore, the interaction between autophagy and insulin function will be examined in this review, particularly in insulin-responsive tissues, such as adipose tissue, liver, and skeletal muscle.

Background: The mu-opioid receptor, encoded by mu-opioid receptor gene (OPRM1), has an important role in the development of addiction to opioids. Its aberrant reduction on the cell membrane is responsible, at least in part, for tolerance and physical dependence. Objectives: The present study was designed to identify the relationship between opium consumption and epigenetic mechanisms involved in opium addiction. Methods: Genomic DNA was extracted from the peripheral blood of 66 men with opium use disorder and 57 healthy men as a control group. Genomic DNAs were treated with sodium bisulfite to convert the un-methylated cytosine to uracil, while methylated cytosine remained unaffected. Nested methylation-specific PCR (MSP) was used for analyses of region 1 (R1) and region 2 (R2) of the OPRM1 promoter DNA methylation. Results: All participants were 19–56 years old, and there was no significant difference in the mean age of both groups (P = 0.082). After Bonferroni correction, results showed that the DNA methylation status significantly increased the risk of opium addiction in the R2 region compared with un-methylation status (OR = 3.80, 95%CI = 1.77–8.17, P = 0.001). However, we found no significant difference in the R1 region DNA methylation between case and control groups (21.2% and 21.1%, respectively) (P = 1). Conclusion: Our findings demonstrated DNA hypermethylation of the R2 region of the OPRM1 promoter in leukocytes of opium use disorder. In peripheral tissues such as blood, changes of epigenetic endpoints with substance use can be considered as potentially clinically useful biomarkers in identifying individuals who may warrant further diagnostic assessment of a substance use disorder.

CD36 is associated with regulation of lipid metabolism, atherosclerosis, and blood pressure. Moreover, its variation may be involved in the development of hypertension and/or coronary artery disease (CAD). The present study was conducted to investigate the possible association of CD36 rs1761667 (G > A) polymorphism with hypertension and/or CAD in the southeastern of Iran. The present observational study was composed of 238 subjects who were admitted for coronary angiography, and divided into four groups: 1) hypertensive without CAD (H-Tens, n = 52); 2) hypertensive with CAD (CAD + H-Tens, n = 57); 3) CAD without hypertension (CAD, n = 65); and 4) non-hypertensive without CAD as the control group (Ctrl, n = 64). The CD36 rs1761667 polymorphism was genotyped with PCR-RFLP method. Association between CD36 rs1761667 genotypes and the risk of CAD and hypertension was assessed using multinomial regression by adjusting for age, sex, creatinine, fasting blood sugar (FBS), systolic blood pressure (SBP) and diastolic blood pressure (DBP). In the present study, minor allele (A) frequency was 0.36. The genotype, but not allele frequency of the CD36 rs1761667 was significantly different between the four study groups (p = 0.003). Furthermore, using a recessive inheritance model CD36 rs1761667 polymorphism was significantly associated with an increased risk of CAD with hypertension (OR = 5.677; 95% CI = 1.053–30.601; p = 0.043). However, using the dominant model of CD36 rs1761667 had a protective effect on H-Tens and CAD patients. The present findings revealed an association between CD36 rs1761667 polymorphism and susceptibility to hypertension and/or CAD in a southeastern Iranian population.