Twins and endocrinology

Kumar, K.V.S. Hari; Modi, Kirtikumar D

doi:10.4103/2230-8210.145074

Cited by 6 publications

(4 citation statements)

References 51 publications

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“…The genetic basis for developing T2DM has been recognized for a long time. The concordance of T2DM in monozygotic twins is ~70.0% compared with 20.0-30.0% in dizygotic twins and a sibling of an affected individual has about three times higher risk for developing the disorder than the general population [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Epigenetic alterations in patients with type 2 diabetes mellitus

Karachanak-Yankova

Dimova

Nikolova

et al. 2015

Balkan Journal of Medical Genetics

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Epigenetic changes, in particular DNA methylation processes, play a role in the pathogenesis and progression of type 2 diabetes mellitus (T2DM) linking genetic and environmental factors. To clarify this role, we have analyzed in patients with different duration of T2DM: (i) expression levels of methyl-CpG-binding domain protein 2 (MBD2) as marker of DNA methylation, and ii) methylation changes in 22 genes connected to cellular stress and toxicity. We have analyzed MBD2 mRNA expression levels in16 patients and 12 controls and the methylation status of stress and toxicity genes in four DNA pools: (i) controls; (ii) newly-diagnosed T2DM patients; (iii) patients with T2DM duration of <5 years and (iv) of >5 years. The MBD2 expression levels were 10.4-times increased on average in T2DM patients compared to controls. Consistent increase in DNA methylation fraction with the increase in T2DM duration was observed in Prdx2 and SCARA3 genes, connected to oxidative stress protection and in BRCA1 and Tp53 tumor-suppressor genes. In conclusion, increased MBD2 expression in patients indicated general dysregulation of DNA methylation in T2DM. The elevated methylation of Prdx2 and SCARA3 genes suggests disturbance in oxidative stress protection in T2DM. The increased methylation of BRCA1 and Tp53 genes unraveled an epigenetic cause for T2DM related increase in cancer risk.

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Section: Introductionmentioning

confidence: 99%

Epigenetic alterations in patients with type 2 diabetes mellitus

Karachanak-Yankova

Dimova

Nikolova

et al. 2015

Balkan Journal of Medical Genetics

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“…The cause of HT and the production of these self-antibodies is still unclear but several genetic factors, environmental factors, and epigenetic factors may play a role [11]. A study conducted by Brix et al showed when comparing monozygotic twins and dizygotic twins, monozygotic twins had a higher concordance rate of HT (50% vs 0 %) and autoantibodies (80% vs 40%) [7,12]. When examining specific alleles, a case-control study showed having HLA-B*46:01 was associated with HT [13].…”

Section: Etiology and Risk Factorsmentioning

confidence: 99%

“…Another study revealed that the prevalence of HT ranged from 4.8-25.8% in women and 0.9-7.9% in men, confirming that HT is more common in women than men [6]. When comparing the concordance rate for monozygotic twins as compared with dizygotic twins, monozygotic had a high rate of 55% vs 0% of the dizygotic twins [7]. With respect to race, Caucasians have the highest rate of developing HT, with a total incidence rate of 5% [8].…”

Section: Introductionmentioning

confidence: 96%

Hashimoto Thyroiditis - A Comprehensive Review

Phagoora,

Saini,

Raghunathan

et al. 2023

PJOM

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Hashimoto thyroiditis (HT) is an inflammatory disorder that often results in hypothyroidism. It has several global implications affecting different regions worldwide. Risk factors for acquiring HT include diet, inheritance, sex, epigenetics, and comorbidities. HT is a complex autoimmune illness characterized by an attack on the thyroid gland by the immune system. At the cellular level, genetic predisposition, environmental triggers, and the loss of immunological tolerance to thyroid antigens all play significant roles in the disease's genesis and progression. There are several mechanisms by which HT may develop, but the typical progression is autoimmune in origin. Many patients do not initially present with symptoms, but later develop symptoms of hypothyroidism. These symptoms include constipation, fatigue, dry skin, weight gain, cold intolerance, decreased energy, memory loss, muscle cramps, hair loss, and irregular menses. Patients with HT usually present with a firm, nontender neck goiter on a physical exam. To distinguish HT from other thyroid pathologies, patient serum should be collected to check for thyroid-specific auto-antibodies against thyroglobulin, thyroid peroxidase, thyroid stimulating hormone. Imaging studies such as ultrasonography with computer-aided techniques using gray-scale features are also diagnostic tools in differentiating between a healthy thyroid and HT. While the most common intervention of HT is synthetic hormone administration with levothyroxine sodium (L-T4), other alternatives or additional treatments include glucocorticoid use, diet alterations, selenium supplementation, vitamin D supplementation, and in more extreme cases, thyroidectomy. While research continues discovering new interventions, each treatment plan is highly variable based on underlying causes and presentations. This comprehensive review hopes to provide an up-to-date compact analysis of literature pertinent to the epidemiology, etiology, risk factors, genetics, pathophysiology, classifications, clinical presentation, diagnosis, and treatments of HT.

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“…[5][6][7] Due to the young age of T1D onset and lower familial clustering than type 2 diabetes, pathogenesis other than gene should be considered in T1D. 8 As known, maternal immune or cytokine changes can be transferred to the fetus through the placenta, thereby affecting fetal development. [9][10][11] Thus, maternal immune related diseases could be important in the cause of T1D.…”

Section: Introductionmentioning

confidence: 99%

Association Between Maternal Mood Disorders and Schizophrenia and the Risk of Type 1 Diabetes in Offspring: A Nationwide Cohort Study

Liu,

Liao,

Chen

et al. 2023

NDT

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Our study aimed to determine whether mothers with bipolar disorder, major depressive disorder, schizophrenia, or schizoaffective disorder affected the risk of type 1 diabetes (T1D) in their offspring. Methods: We conducted a nationwide cohort study by using data from Taiwan's National Health Insurance Research Database and the Maternal and Child Health Database from 2004 to 2018. A total of 2,556,640 mother-child pairs were identified. Cox proportional hazards models were used to compare the risk of T1D between children born to mothers with mood disorders and schizophrenia and those without. Results: No significant difference in risk of T1D was observed between the offspring of mothers with major psychiatric disorders and those without (adjusted hazard ratio (aHR) of 0.86 with a 95% confidence interval (CI) of 0.58-1.24). In subgroup analysis, we found an aHR of 1.81 with a 95% CI of 0.83-3.82 in the maternal bipolar disorder on the risk of T1D in offspring and an aHR of 0.87 (95% CI: 0.59-1.25) in maternal major depressive disorder. In the schizophrenia/schizoaffective disorder group, aHR cannot be obtained due to lesser than three events in the analysis. Conclusion:The risk of T1D in offspring of mothers with mood disorders and schizophrenia was not significant. However, children born to mothers with bipolar disorder may have a tendency to develop T1D. The relationship between maternal psychiatric disorders and the risk of T1D in offspring warrants further investigation in studies with longer follow-up periods.

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Twins and endocrinology

Cited by 6 publications

References 51 publications

Epigenetic alterations in patients with type 2 diabetes mellitus

Epigenetic alterations in patients with type 2 diabetes mellitus

Hashimoto Thyroiditis - A Comprehensive Review

Association Between Maternal Mood Disorders and Schizophrenia and the Risk of Type 1 Diabetes in Offspring: A Nationwide Cohort Study

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