Early-life exposure to the Chinese famine, genetic susceptibility and the risk of type 2 diabetes in adulthood

Diabetologia ◽  
2021 ◽  
Author(s):  
Bin Wang ◽  
Jing Cheng ◽  
Heng Wan ◽  
Yuying Wang ◽  
Wen Zhang ◽  
...  
Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4063
Author(s):  
Jing Liu ◽  
Guimin Wang ◽  
Yiling Wu ◽  
Ying Guan ◽  
Zhen Luo ◽  
...  

Background: Early-life exposure to the Chinese famine has been related to the risk of obesity, type 2 diabetes, and nonalcoholic fatty liver disease later in life. Nevertheless, the long-term impact of famine exposure on metabolic associated fatty liver disease (MAFLD), a recently proposed term to describe liver disease associated with known metabolic dysfunction, remains unknown. The aim of our study was to explore the relationship between early famine exposure and MAFLD in adulthood. Methods: A total of 26,821 participants (10,994 men, 15,827 women) were recruited from a cohort study of Chinese adults in Shanghai. We categorized participants into four famine exposure subgroups based on the birth year as nonexposed (1963–1967), fetal-exposed (1959–1962), childhood-exposed (1949–1958), and adolescence-exposed (1941–1948). MAFLD was defined as liver steatosis detected by ultrasound plus one of the following three criteria: overweight/obesity, type 2 diabetes, or evidence of metabolic dysregulation. Multivariable logistic regression models were performed to examine the association between famine exposure and MAFLD. Results: The mean ± standard deviation age of the participants was 60.8 ± 6.8 years. The age-adjusted prevalence of MAFLD was 38.3, 40.8, 40.1, and 36.5% for the nonexposed, fetal-exposed, childhood-exposed, and adolescence-exposed subgroups, respectively. Compared with nonexposed participants, fetal-exposed participants showed an increased risk of adulthood MAFLD (OR = 1.10, 95% CI 1.00–1.21). The significant association between fetal famine exposure and MAFLD was observed in women (OR = 1.22, 95% CI 1.08–1.37), but not in men (OR = 0.88, 95% CI 0.75–1.03). In age-balanced analyses combining pre-famine and post-famine births as the reference, women exposed to famine in the fetal stage still had an increased risk of MAFLD (OR = 1.15, 95% CI 1.05–1.26). Conclusions: Prenatal exposure to famine showed a sex-specific association with the risk of MAFLD in adulthood.


2015 ◽  
Vol 19 (4) ◽  
pp. 230-237 ◽  
Author(s):  
Manshu Song ◽  
Feifei Zhao ◽  
Longjin Ran ◽  
Mamatyusupu Dolikun ◽  
Lijuan Wu ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Masakazu Nishigaki ◽  
Eiko Sato ◽  
Ryota Ochiai ◽  
Taiga Shibayama ◽  
Keiko Kazuma

Background. Offspring of type 2 diabetic patients are at a high risk of type 2 diabetes. Information on diabetes genetic susceptibility and prevention should be supplied to the offspring.Methods. A six-page booklet on diabetes genetic susceptibility and prevention was distributed to 173 patients who ere ordered to hand it to their offspring. The patients answered a self-administered questionnaire on booklet delivery and attitudinal and behavioral changes toward diabetes and its prevention in themselves and their offspring.Results. Valid responses were obtained from 130 patients. Forty-nine patients had actually handed the booklet. Booklet induces more relief than anxiety. From the patient's view, favorable attitudinal and/or behavioral changes occurred in more than half of the offspring who were delivered the booklet.Conclusion. The booklet worked effectively on attitudes and behaviors toward diabetes and its prevention both in patients and their offspring. However, the effectiveness of patients as information deliverers was limited.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Yanping Li ◽  
Qibin Qi ◽  
Tsegaselassie Workalemahu ◽  
Frank B Hu ◽  
Lu Qi

Background: Both stressful intrauterine milieus and genetic susceptibility have been linked to later life diabetes risk. The present study aims to examine the interaction between low birth weight, a surrogate measure of stressful intrauterine milieus, and genetic susceptibility in relation to risk of type 2 diabetes in adulthood. Methods: The analysis included two independent, nested case-control studies of in total 2591 cases of type 2 diabetes and 3052 healthy controls from prospective cohorts: the Nurses’ Health Study (NHS) and the Health Professionals Follow-up Study (HPFS). We developed 2 genotype scores using susceptibility loci recently identified through Genome Wide Association Studies: 1) an ‘obesity genotype score’ based on 32 BMI-predisposing single nucleotide polymorphisms (SNPs); and 2) a ‘diabetes genotype score’ based on 35 diabetes-predisposing SNPs. Results: Both the obesity genotype score and diabetes genotype score showed consistently significant association with risk of type 2 diabetes in NHS and HPFS ( P for trend < 0.01). In the pooled sample of the two cohorts, we found significant interaction between birth weight and obesity genotype score in relation to type 2 diabetes ( P for interaction=0.017). In low birth weight individuals (≤ 2.5 kg), the multivariable-adjusted odds ratio (OR) was 2.55 (95% confidence interval [CI]: 1.34–4.84) in the comparison of the highest with the lowest quartile of the obesity genotype score, while the OR was 1.27 (95%CI: 1.04–1.55) among individuals with birth weight above 2.5kg. Diabetes genotype score also showed stronger association with type 2 diabetes risk in individuals with low birth weight than those with high birth weight. Comparing individuals of the highest with the lowest quartile of the diabetes genotype score, the multivariable-adjusted odds ratio was 3.80 (95%CI: 1.76–8.24) among individuals with low birth weight and was 2.27 (95%CI: 1.82–2.83) among those with high birth weight. However, test for interaction was marginal ( P =0.16). Conclusion: Our data suggest low birth weight and genetic susceptibility to obesity may synergistically affect adulthood risk of type 2 diabetes.


Diabetologia ◽  
2019 ◽  
Vol 62 (10) ◽  
pp. 1891-1900
Author(s):  
Sarah-Naomi James ◽  
Andrew Wong ◽  
Therese Tillin ◽  
Rebecca Hardy ◽  
Nishi Chaturvedi ◽  
...  

Author(s):  
Ivonne P. M. Derks ◽  
Annemarie Koster ◽  
Miranda T. Schram ◽  
Coen D. A. Stehouwer ◽  
Pieter C. Dagnelie ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-17 ◽  
Author(s):  
Delphine Fradin ◽  
Pierre Bougnères

Type 2 Diabetes Mellitus (T2DM) is a metabolic disorder influenced by interactions between genetic and environmental factors. Epigenetics conveys specific environmental influences into phenotypic traits through a variety of mechanisms that are often installed in early life, then persist in differentiated tissues with the power to modulate the expression of many genes, although undergoing time-dependent alterations. There is still no evidence that epigenetics contributes significantly to the causes or transmission of T2DM from one generation to another, thus, to the current environment-driven epidemics, but it has become so likely, as pointed out in this paper, that one can expect an efflorescence of epigenetic knowledge about T2DM in times to come.


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