Abstract
ObjectivesFamine exposure in early life was associated with type 2 diabetes, non-alcoholic fatty liver disease and metabolic syndrome, etc. But evidence in early famine exposure and insulin resistance and beta cell dysfunction were limited. We aimed to investigate whether the association existed between famine exposure in early life and beta cell dysfunction and insulin resistance in adulthood.MethodsIn all, 7912 non-diabetic participants were included in this study, based on SPECT-China study. Participants with fetal or childhood famine exposure (birth year 1949–1962) were exposure group. Insulin resistance was estimated by the homeostasis model assessment index of insulin resistance (HOMA-IR). Beta cell function, represented by insulin secretion, was estimated by the disposition index. The associations of famine exposure with HOMA-IR and disposition index were assessed via linear regression.ResultsIn men, we did not observe a significant association between early life famine exposure and ln(HOMA-IR) in all three models (P > 0.05 for all). However, in women, early life famine exposure were found to have significant association with ln(HOMA-IR) after adjustments for urbanization, severity of famine exposure, current smoker, waist circumference, hypertension, and dyslipidemia (unstandardized coefficients 0.055, 95% confidence interval 0.021, 0.088, P = 0.001). Early life famine exposure was observed to be negatively associated with ln(disposition index) after adjustments for the above potential confounders, both in men (model 3: unstandardized coefficients −0.042, 95% confidence interval −0.072,−0.012, P = 0.006) and women (model 3: unstandardized coefficients −0.033, 95% confidence interval −0.058,−0.009, P = 0.008).ConclusionsIn conclusion, exposure to famine in fetal- and childhood- life period is associated with beta cell dysfunction in males and females without diabetes, but early life famine exposure was only associated with insulin resistance in non-diabetic females. These results indicate that malnutrition in early life period may offer a modifiable factor for type 2 diabetes development.
Highlights
Insulin resistance and beta cell dysfunction are regarded as critical contributors to the progression of several highly prevalent glucose metabolic disorders, including diabetes, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD)[1,2,3,4,5]
In men, compared to the non-exposed subjects, the waist circumference of famine exposed subjects was significantly lower (P = 0.049), while the level of homeostasis model assessment index of insulin resistance (HOMA-IR) and disposition index, and the prevalence of hypertension and dyslipidemia were comparable between famine exposed and age-balanced non-exposed group
We did not observe a significant association between early life famine exposure and ln(HOMA-IR) in all three models (P > 0.05 for all)
Summary
Insulin resistance and beta cell dysfunction are regarded as critical contributors to the progression of several highly prevalent glucose metabolic disorders, including diabetes, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD)[1,2,3,4,5]. The studies show consistent associations between prenatal famine and adult body size, diabetes, and schizophrenia[14] These associations could be explained by the Developmental Origins of Health and Disease (DOHaD) hypothesis. DOHaD postulates that adverse events occur during early phases of human development affect the pattern of health and disease throughout life, especially chronic and metabolic diseases[15]. Exposure to this national calamity was reported to have close association with NAFLD, metabolic syndrome, and visceral adipose dysfunction in adulthood in our previous studies[16,17,18], and was found to exacerbate the association between hypertension and cardiovascular disease[19]
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