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Background Maternal obesity is a global health concern that leads to metabolic alterations in the offspring, making them vulnerable to metabolic disorders in adulthood. Early identification of such neonates would provide opportunities to positively alter modifiable risk factors for non-communicable diseases (NCDs) to prevent their occurrence later in life. Objectives This study aimed to assess and contrast insulin resistance (IR) levels in neonates born to mothers with obesity and those born to healthy, non-obese mothers. Methods This case-control study was conducted after approval from the institutional ethics committee. A total of 98 healthy, non-obese pregnant females were included in Group 1, and 68 obese pregnant females were included in Group 2. The participants were followed up until delivery and cord blood samples were collected after delivery. Neonatal glucose and insulin concentrations were estimated, and indices of IR such as homeostatic model assessment for insulin resistance (HOMA-IR), quantitative insulin-sensitivity check index (QUICKI), and glucose-to-insulin ratio were calculated. Neonatal IR indices and anthropometric measurements were compared between the groups using the Z test and correlated with the maternal pre-pregnancy body mass index (BMI) using Pearson's correlation. Additionally, Pearson's correlations were examined between neonatal IR indices and anthropometric measurements. Statistical significance was set at p <0.05. Results Neonates in Group 2 exhibited significantly higher anthropometric parameters and IR indices than those in Group 1. A statistically significant positive correlation was identified between maternal pre-pregnancy BMI, neonatal anthropometric parameters, and IR. Furthermore, a statistically significant positive correlation was observed between neonatal IR and the anthropometric parameters. Conclusion Neonates born to obese mothers exhibited higher anthropometric parameters and insulin resistance than those born to non-obese, healthy mothers. Assessment of IR at birth can help identify neonates who are at higher risk of developing NCD in later life. Timely promotion of a healthy lifestyle can reduce the occurrence of NCDs in later life.
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BACKGROUND: Empirical use of potentially hepatotoxic drugs in the management of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is considered as one of the major etiopathogenetic factors for liver injury. Recent evidence has shown that an underlying genetic factor may also occur. Hence, it is important to understand the host genetics and iatrogenic-based mechanisms for liver dysfunction to make timely remedial measures. AIM: To investigate drug-induced and genetic perspectives for the development of coronavirus disease 2019 (COVID-19)-related liver injury. METHODS: Reference Citation Analysis, PubMed, Google Scholar and China National Knowledge Infrastructure were searched by employing the relevant MeSH keywords and pertaining data of the duration, site and type of study, sample size with any subgroups and drug-induced liver injury outcome. Genetic aspects were extracted from the most current pertinent publications. RESULTS: In all studies, the hepatic specific aminotransferase and other biochemical indices were more than their prescribed upper normal limit in COVID-19 patients and were found to be significantly related with the gravity of disease, hospital stay, number of COVID-19 treatment drugs and worse clinical outcomes. In addition, membrane bound O-acyltransferase domain containing 7 rs641738, rs11385942 G>GA at chromosome 3 gene cluster and rs657152 C>A at ABO blood locus was significantly associated with severity of livery injury in admitted SARS-CoV-2 patients. CONCLUSION: Hepatic dysfunction in SARS-CoV-2 infection could be the result of individual drugs or due to drug-drug interactions and may be in a subset of patients with a genetic propensity. Thus, serial estimation of hepatic indices in hospitalized SARS-CoV-2 patients should be done to make timely corrective actions for iatrogenic causes to avoid clinical deterioration. Additional molecular and translational research is warranted in this regard.
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BACKGROUND: Purpose of insulin resistance (IR) adapted by mother is to deliver enough quantity of nutrients to the growing fetus. Many maternal hormones and factors play role in causation of IR during pregnancy. AIM: The study aims at evaluating IR at different trimesters of pregnancy. MATERIALS AND METHODS: Pregnant women at 1(st), 2(nd) and 3(rd) trimester were grouped into groups I, II and III respectively (n=20 in each group). Healthy non-pregnant women were taken as controls (n=30). Fasting plasma glucose (FPG) and fasting serum insulin (FSI) were measured and IR indices such as fasting glucose to insulin ratio (FGIR), quantitative insulin sensitivity check index (QUICKI), log FSI and log HOMA1-IR were calculated. The student's t-test and one way Analysis of variance (ANOVA) were used for data analysis. RESULTS: The mean FSI, log FSI and log HOMA 1-IR were significantly higher in 2(nd) and 3(rd) trimesters while QUICKI was significantly lower in 2(nd) and 3(rd) trimesters of pregnancy when compared with controls. Also, mean FGIR was found to be significantly lower in 3rd trimester when compared with controls. CONCLUSION: As pregnancy advances, IR increases. Increased IR is associated with poor maternal and fetal outcome. Screening of all pregnancy for IR and early intervention may help to reduce the associated complications.