Exposure to severe famine in the prenatal or postnatal period and the development of diabetes in adulthood: an observational study

Wang, Ningjian; Cheng, Jing; Han, Bing; Qin, Li; Chen, Yi; Xia, Fangzhen; Jiang, Boren; Jensen, Michael D.; Lu, Yingli

doi:10.1007/s00125-016-4148-4

Cited by 80 publications

(76 citation statements)

References 29 publications

(52 reference statements)

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“…Interestingly, the timing of association between the famine exposure in early life and adult T2D was gender-specific: an elevated risk of T2D development was evident in the foetal-exposed men (OR = 1.64) and childhood-exposed women (OR = 2.81). These findings were further confirmed in subsequent research by the same authors, where a significant association between the famine severity in the areas of exposure and the risk of T2D was found [71]. Those subjects who were exposed to severe famine during the foetal and childhood periods had substantially higher odds estimates (1.90 and 1.44, respectively).…”

Section: Quasi-experimental Design In Studying the Developmental Osupporting

confidence: 71%

Early-Life Nutritional Programming of Type 2 Diabetes: Experimental and Quasi-Experimental Evidence

Vaiserman

2017

Nutrients

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Consistent evidence from both experimental and human studies suggest that inadequate nutrition in early life can contribute to risk of developing metabolic disorders including type 2 diabetes (T2D) in adult life. In human populations, most findings supporting a causative relationship between early-life malnutrition and subsequent risk of T2D were obtained from quasi-experimental studies (‘natural experiments’). Prenatal and/or early postnatal exposures to famine were demonstrated to be associated with higher risk of T2D in many cohorts around the world. Recent studies have highlighted the importance of epigenetic regulation of gene expression as a possible major contributor to the link between the early-life famine exposure and T2D in adulthood. Findings from these studies suggest that prenatal exposure to the famine may result in induction of persistent epigenetic changes that have adaptive significance in postnatal development but can predispose to metabolic disorders including T2D at the late stages of life. In this review, quasi-experimental data on the developmental programming of T2D are summarized and recent research findings on changes in DNA methylation that mediate these effects are discussed.

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Section: Quasi-experimental Design In Studying the Developmental Osupporting

confidence: 71%

Early-Life Nutritional Programming of Type 2 Diabetes: Experimental and Quasi-Experimental Evidence

Vaiserman

2017

Nutrients

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“…The data are from 10,441 participants of SPECT‐China, a cross‐sectional survey in East China (ChiCTR‐ECS‐14005052, http://www.chictr.org.cn). Recruitment and enrollment have been previously described in detail (Wang, Cheng, et al, ; Wang et al, ; Wang, Wang, et al, ). A total of 3,226 postmenopausal women were selected.…”

Section: Methodsmentioning

confidence: 99%

Follicle‐stimulating hormone promotes renal tubulointerstitial fibrosis in aging women via the AKT/GSK‐3β/β‐catenin pathway

et al. 2019

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Estrogen withdrawal in aging women contributes to the progression of chronic kidney disease (CKD). However, the effect of high circulating follicle‐stimulating hormone (FSH) levels on renal dysfunction remains unknown. In this study, blood samples from 3,055 postmenopausal women were collected and tested, which showed that there was a strong negative correlation between eGFR and FSH levels (p < 0.001), independent of LH, testosterone, and estradiol. Functional FSHR was detected in renal tubular epithelial cells. In vivo, high circulating FSH levels promoted a phenotype of tubulointerstitial fibrosis, characterized by increases in 24‐hr urine protein/creatinine ratio, serum Cr, serum BUN, and ECM deposition. Similar results obtained from cultured HK‐2 cells showed that FSH increased the transcriptional and protein expression of profibrotic mediators (collagen IV, fibronectin, and PAI‐1). This promotion of fibrosis by FSH occurred through the activation of AKT/GSK‐3β/β‐catenin pathway, which could be attenuated by silencing FSHR by siRNA or by LY294002 or MK2206. In addition, FSH‐stimulated HK‐2 cells secreted IL‐8, which promoted macrophage migration to exacerbate tubulointerstitial fibrosis. These results revealed a previously unknown effect of FSH on kidney injury, which may offer a critical insight into the development of CKD in aging postmenopausal women.

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“…SCZ and T2D are contributed by an interaction of environmental and genetic risk factors. Prenatal famine is a common environmental factor associated with T2D and SCZ risk (Wang & Zhang, ; N. Wang et al, ). Furthermore, several possible SCZ‐pathways (Dean, ; Javitt, ) may contribute to T2D and MetS.…”

Section: Mental and Metabolic Comorbiditymentioning

confidence: 99%

Co‐shared genetics and possible risk gene pathway partially explain the comorbidity of schizophrenia, major depressive disorder, type 2 diabetes, and metabolic syndrome

Postolache

Bosque-Plata

Jabbour

et al. 2019

American J of Med Genetics Pt B

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Schizophrenia (SCZ) and major depressive disorder (MDD) in treatment-naive patients are associated with increased risk for type 2 diabetes (T2D) and metabolic syndrome (MetS). SCZ, MDD, T2D, and MetS are often comorbid and their comorbidity increases cardiovascular risk: Some risk genes are likely co-shared by them. For instance, transcription factor 7-like 2 (TCF7L2) and proteasome 26S subunit, non-ATPase 9 (PSMD9) are two genes independently reported as contributing to T2D and SCZ, and PSMD9 to MDD as well. However, there are scarce data on the shared genetic risk among SCZ, MDD, T2D, and/or MetS. Here, we briefly describe T2D, MetS, SCZ, and MDD and their genetic architecture. Next, we report separately about the comorbidity of SCZ and MDD with T2D and MetS, and their respective genetic overlap. We propose a novel hypothesis that genes of the prolactin (PRL)-pathway may be implicated in the comorbidity of these disorders. The inherited predisposition of patients with SCZ and MDD to psychoneuroendocrine dysfunction may confer increased risk of T2D and MetS. We illustrate a strategy to identify risk variants in each disorder and in their comorbid psychoneuroendocrine and mentalmetabolic dysfunctions, advocating for studies of genetically homogeneous and phenotype-rich families. The results will guide future studies of the shared predisposition and molecular genetics of new homogeneous endophenotypes of SCZ, MDD, and metabolic impairment.

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Exposure to severe famine in the prenatal or postnatal period and the development of diabetes in adulthood: an observational study

Abstract: Exposure to severe famine in the fetal or childhood period may predict a higher HbA and an increased diabetes risk in adulthood. These results from China indicate that both the prenatal and postnatal period may offer critical time windows for the determination of the risk of diabetes.

Cited by 80 publications

References 29 publications

Early-Life Nutritional Programming of Type 2 Diabetes: Experimental and Quasi-Experimental Evidence

Early-Life Nutritional Programming of Type 2 Diabetes: Experimental and Quasi-Experimental Evidence

Follicle‐stimulating hormone promotes renal tubulointerstitial fibrosis in aging women via the AKT/GSK‐3β/β‐catenin pathway

Co‐shared genetics and possible risk gene pathway partially explain the comorbidity of schizophrenia, major depressive disorder, type 2 diabetes, and metabolic syndrome

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