On behalf of the IFCC organization, I am delighted to extend my heartfelt congratulations to the Iranian Biochemical Society (IBS) for its illustrious history and commendable plans to relaunch Acta Biochimica Iranica. As a pioneer, the Iranian Biochemical Society was the first society in the Middle East to become a full-fledged national society member of IFCC in the 1960s, standing as the premier and most dynamic society in the region dedicated to advancing biochemical education and research. A significant milestone occurred in 1962 when the IBS initiated the publication of Acta Biochimica Iranica, an international journal that persisted until 1972. This historical endeavor underscores the prominent leadership role the Iranian society undertook in the realm of biochemistry several decades ago and serves as a testament to its esteemed legacy.

Objectives: Preeclampsia (PE) is a pregnancy-related disorder with an incidence of 2-5% that causes the death of 40,000 women worldwide each year. Among different accepted etiologies, hyperhomocysteinemia has been shown to be a key player in the progression of PE. Considering the solid role of methylenetetrahydrofolate reductase (MTHFR) in the metabolism of homocysteine, genetic polymorphism of MTHFR that could affect its activity may trigger the risk of PE. This hierarchical Bayesian metaanalysis aimed to assess the possible association between C677T MTHFR polymorphism and the risk of PE.

 Methods: In this study, PubMed, Scopus, and Web of Science databases were searched from 2000 until 2019 to evaluate the association of MTHFR C677T polymorphism with the risk of PE in relevant case-control studies. The relevant studies were included regardless of population ethnicity and geographical limitation. The extracted data were statistically analyzed using a hierarchical Bayesian method and the association strength was estimated by log (OR) with a 95% credible interval.

Results: Thirty-three studies with 3930 cases and 5236 controls met our inclusion criteria. The pooled results indicated no significant effect of MTHFR C677T (C>T) on PE risk under allelic (log(OR) = 0.09, 95% CI = -0.02, 0.204), homozygous (log(OR) = 0.173, 95% CI = -0.027, 0.378), heterozygous (log(OR) = -0.009, 95% CI = -0.123, 0.104), dominant (log(OR) = 0.009, 95% CI = -0.109, 0.133), and recessive (log(OR) = 0.173, 95% CI = -0.012, 0.366) models.

 Conclusion: It can be concluded that MTHFR C677T polymorphism had no significant effect on the risk of PE.

Cardiovascular diseases (CVDs) are the major cause of death in both developed and developing countries. It is widely accepted that predicting CVDs in the early stages or before the onset of the diseases could be a central goal in the management, prevention, and treatment of these diseases. Adipokines, a large and diverse group of molecules secreted by adipose tissue that affect cardiovascular function, have played a crucial role in the cardiovascular system. C1q/tumor necrosis factor-related protein (CTRP) is a newly discovered family of adipokines that are paralogs of adiponectin. This family includes 15 members (CTRP1 to CTRP15). Recent studies have shown that CTRPs have diverse biological effects on the cardiovascular system. In this review, recent research on the expression of the CTRP gene superfamily in CVDs is examined to assess their potential as new CVD biomarkers. Given the growing data on the roles of CTRPs in the physiology and development of CVDs, this review discusses the role of various types of CTRPs, including CTRP1, CTRP2, CTRP3, CTRP6, CTRP9, CTRP12, and CTRP13 in the management, prevention, and treatment of CVDs.

Objectives: The K121Q polymorphism of the Ectoenzyme Nucleotide Pyrophosphate Phosphodiesterase 1 (ENPP1) gene has been variably associated with obesity in several populations. However, this association has not been studied in Iranian subjects. It was hypothesized that the K121Q variant might be associated with obesity and related risk factors in subjects with normal glucose tolerance and normal fasting glucose.

Methods: The K121Q genotypes were determined by PCR-restriction fragment length polymorphism in 377 non-diabetic subjects.

Results: In males, the frequency of the Q allele was 20.8% and 15.9% (p=0.269) in obese and non-obese subjects, respectively. The ENPP1 genotype (KQ+QQ) was not associated with systolic and diastolic blood pressure, triglyceride, cholesterol, LDL-C, HDL-C, HOMA-IR, or insulin levels in both genders. Male carriers of the KQ+QQ genotype had significantly higher values for BMI (p=0.079), waist (p=0.01), and WHR (p=0.006) than subjects with the KK genotype. Obesity-related parameters were not significantly different between obese and non-obese female subjects.

Conclusion: Our results suggest that the ENPP1 121Q allele might be associated with obesity and related parameters only among Iranian normoglycemic male subjects.

Objectives: Women with Polycystic Ovary Syndrome (PCOS) are more prone to adverse outcomes, including hypertension, obesity, hyperlipidemia, insulin resistance, type 2 diabetes mellitus, metabolic syndrome, and cardiovascular disease. This study examined the potential link between abnormal steroid hormone levels and insulin resistance (IR) in reproductive-aged women with PCOS.

Methods: This study involved 61 participants: a case group of 33 patients with confirmed PCOS based on Rotterdam criteria and a control group of 28 healthy individuals without PCOS. Steroid hormone levels, IR indices, metabolic markers, and demographic characteristics of participants were measured.

Results: The results showed significant differences in testosterone (P=0.018), dihydrotestosterone (DHT) (P=0.009), and androstenedione (P=0.002) levels between the two groups. Insulin levels and HOMA-IR were significantly higher in the patients (P=0.034 and 0.025, respectively). Significant correlations were found between androstenedione and insulin (P=0.021), fasting blood sugar, and homeostatic model assessment of insulin resistance (HOMA-IR) levels (P=0.001), as well as between DHT level and IR indices (P=0.03). Additionally, patients with PCOS had higher diastolic blood pressure and lower levels of T4.

Conclusion: The findings of this study showed higher androgen levels in PCOS patients and a significant correlation between DHT and androstenedione levels with IR indices in PCOS patients, which establishes a remarkable connection between hyperandrogenism and insulin resistance in PCOS.

Resveratrol has been reported to decrease lipid accumulation in the liver, but the molecular mechanism underlying this effect remains unknown. In this study, the role of autophagy in high glucose (HG)-induced lipogenesis in the presence of resveratrol in HepG2 cells was investigated. Resveratrol pretreatment prevented HG-induced total lipid content, triglyceride level, apo B secretion, and key lipogenic gene expression (FAS, ACC, SREBP1c, and MTP). HG diminished p-Foxo1 and p-AMPK levels, while resveratrol reversed this effect by inducing p-Foxo1 and p-AMPK levels by 40% and 47%, respectively. HG treatment reduced autophagy markers such as LC3-II, ATG5, and ATG7 and increased p62 protein levels, whereas resveratrol significantly reversed these effects. Additionally, inhibiting autophagy with chloroquine led to enhanced total lipid and triglyceride content compared to untreated control cells. Notably, co-treatment with chloroquine inhibited the preventive effect of resveratrol on HG-induced lipogenesis in HepG2 cells. Furthermore, while HG induced p-mTOR level in HepG2 cells, resveratrol reversed this effect. Rapamycin, an inhibitor of mTOR, ameliorated HG-induced total lipid and triglyceride content and the expression of lipogenic genes. Collectively, these data demonstrate that the lipid-lowering effect of resveratrol is mediated through the induction of autophagy in an mTOR-dependent mechanism.

Objectives: Previous works have linked high concentrations of glucose to cellular toxicity through autophagy modulation. However, the ways in which high glucose (HG) regulates inflammation and apoptosis in peripheral blood mononuclear cells (PBMCs) have not been well characterized.
Methods: In the present study, the role of autophagy in inflammatory responses and apoptotic death of PBMCs exposed to HG was investigated.
Results: 33mM glucose (HG) increased the level of LC3-II at 12h, 24h, and 48h. NH4Cl, a lysosome inhibitor that can block autophagic flux, further promoted LC3-II accumulation in HGtreated cells at 12h, 24h, and 48h. The protein level of p62 significantly decreased from 12h to 48h in HG-treated cells, suggesting an induction of autophagic flux in HG-treated PBMCs. Inhibiting autophagy with chloroquine (CQ) significantly augmented HGinduced PBMCs apoptotic death, as demonstrated by increased cleaved PARP and Cyt C levels and an increased percentage of apoptotic (YO-PRO-1 positive and PI negative) cells. Furthermore, CQ pretreatment exacerbated HG-induced TNF-α, IL-6, and IL-1β mRNA expression in PBMCs.
Conclusion: The data revealed that the autophagy system could be activated in HG-treated PBMCs. The results also indicated that the induction of autophagy might play an adaptive and protective role in HG-induced inflammation and apoptotic death of PBMCs.