scholarly journals Maternal High-Fiber Diet Protects Offspring against Type 2 Diabetes

Nutrients ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 94
Author(s):  
Huishi Toh ◽  
James A. Thomson ◽  
Peng Jiang

Previous studies have reported that maternal malnutrition is linked to increased risk of developing type 2 diabetes in adulthood. Although several diabetic risk factors associated with early-life environment have been identified, protective factors remain elusive. Here, we conducted a longitudinal study with 671 Nile rats whereby we examined the interplay between early-life environment (maternal diet) and later-life environment (offspring diet) using opposing diets that induce or prevent diet-induced diabetes. Specifically, we modulated the early-life environment throughout oogenesis, pregnancy, and nursing by feeding Nile rat dams a lifelong high-fiber diet to investigate whether the offspring are protected from type 2 diabetes. We found that exposure to a high-fiber maternal diet prior to weaning significantly lowered the risk of diet-induced diabetes in the offspring. Interestingly, offspring consuming a high-fiber diet after weaning did not develop diet-induced diabetes, even when exposed to a diabetogenic maternal diet. Here, we provide the first evidence that the protective effect of a high-fiber diet can be transmitted to the offspring through the maternal diet, which has important implications in diabetes prevention.

2020 ◽  
Author(s):  
Huishi Toh ◽  
James A. Thomson ◽  
Peng Jiang

AbstractPrevious studies have reported that maternal malnutrition is linked to increased risk of developing type 2 diabetes in adulthood. Although several diabetic risk factors associated with early life environment have been identified, protective factors remain elusive. Here, we modulate the early life environment using a maternal high fiber diet to investigate whether the offspring are protected from type 2 diabetes. We examined the interplay between early life environment (maternal diet) and later life environment (offspring diet) using a longitudinal study with 671 Nile rats. We found that exposure to a high fiber maternal diet prior to weaning significantly lowers the risk of diet-induced diabetes in the offspring. Interestingly, offspring consuming a high fiber diet after weaning do not get diet-induced diabetes, even when exposed to a diabetogenic maternal diet. Here, we provide the first evidence that the protective effect of high fiber can be transmitted to the offspring through a maternal diet, which has important implications in diabetes prevention.


2016 ◽  
Vol 7 (5) ◽  
pp. 505-512 ◽  
Author(s):  
S. Firmin ◽  
N. Bahi-Jaber ◽  
L. Abdennebi-Najar

It is now accepted that the way our health evolves with aging is intimately linked to the quality of our early life. The present review highlights the emerging data of Developmental Origins of Health and Disease field on developmental disruption by toxicants and their subsequent effect on type 2 diabetes. We report adverse neonatal effects of several food contaminants during pregnancy and lactation, among them bisphenol A, chlorpyrifos, perfluorinated chemicals on pancreas integrity and functionality in later life. The described alterations, in conjunction with disruption of β cell mass in early life, can lead to dysregulation of glucose metabolism, insulin synthesis, which facilitates the development of insulin resistance and progression of diabetes in the adult. Despite limited and often inconclusive epidemiologic and experimental data, more recent data clearly show that infants appear to be at increased risk of type 2 diabetes in later life. This may be a result of continued exposure to chemical food contaminants during the critical window of pancreas development. In societies already burdened with increased incidence of non-communicable chronic diseases, there is a clear need for information regarding the potential harmful effects of chemical food contaminants on adult health diseases.


Diabetes Care ◽  
2009 ◽  
Vol 32 (6) ◽  
pp. 990-995 ◽  
Author(s):  
M. Shah ◽  
M. Chandalia ◽  
B. Adams-Huet ◽  
L. J. Brinkley ◽  
K. Sakhaee ◽  
...  

2002 ◽  
Vol 75 (6) ◽  
pp. 1023-1030 ◽  
Author(s):  
Thomas MS Wolever ◽  
Katrin B Schrade ◽  
Janet A Vogt ◽  
Elizabeth B Tsihlias ◽  
Michael I McBurney

2007 ◽  
Vol 6 (2) ◽  
pp. 111-116 ◽  
Author(s):  
R.T. Ikem . ◽  
B.A. Kolawole . ◽  
E.O. Ojofeitimi . ◽  
A. Salawu . ◽  
O.A. Ajose . ◽  
...  

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Cyril WC Kendall ◽  
Livia S Augustin ◽  
Sandra Mitchell ◽  
Sandhya Sahye-Pudaruth ◽  
Judy Coveney ◽  
...  

2017 ◽  
Vol 8 (5) ◽  
pp. 513-519 ◽  
Author(s):  
T. Bianco-Miotto ◽  
J. M. Craig ◽  
Y. P. Gasser ◽  
S. J. van Dijk ◽  
S. E. Ozanne

Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.


1970 ◽  
Vol 24 (1) ◽  
pp. 16-20 ◽  
Author(s):  
MT Rahman ◽  
T Tahmin ◽  
S Ferdousi ◽  
SN Bela

Gestational Diabetes Mellitus (GDM) is a very common and important disease occurring during pregnancy and has detrimental effect on both the mother and the baby. The mother is at increased risk of developing obstetric complications like prolonged labour, prone to develop type 2 diabetes in future and the baby is born with overweight, cause of childhood obesity and later life development of type 2 diabetes. A short review and current concept of GDM is discussed. Key words: GDM, Type 2 diabetes, Obesity, Macrosomia, Complications   doi: 10.3329/bjpath.v24i1.2877 Bangladesh J Pathol 24 (1) : 16-20


2021 ◽  
Author(s):  
Feng Ning ◽  
Jing Zhao ◽  
Yanlei Zhang ◽  
Lei Zhang ◽  
Xin Song ◽  
...  

Abstract Background: This study will investigate effect of famine exposure in early life associated with the risk of type 2 diabetes in adulthood during the Chinese Famine.Methods: A total of 3,418 individuals aged 35-74 years free of diabetes in 2006 and in 2009 study surveys, were prospectively followed up to 2009 and 2012, respectively. Individuals were grouped into non-exposed (1962-1978), fetal-exposed (1959-1961), childhood-exposed (1949-1958) and adolescence/adult-exposed cohorts (1931-1948). Logistic regression model was employed to assess effect of famine exposure on diabetes incidence, adjusting for potential covariates.Results: During a mean follow up of 3 years, the age-adjusted cumulative incidences of type 2 diabetes were 6.3%, 13.0% 11.0% and 13.8% in non-exposed, fetal, child and adolescence/adult-exposed cohorts, respectively (P=0.026). Compared with non-exposed individuals, relative risks (95% confidence intervals) for diabetes incidence were 2.15(1.29-3.60), 1.53(0.93-2.51), and 1.65(0.75-3.63) in those exposure in fetal, child and adolescence/adult, controlling for covariates. The interactions between famine exposure and obesity, education, family history of diabetes were not observed, except for famine exposure and residential areas. Individuals lived in rural areas increased risk for type 2 diabetes in fetal and child exposure, with an incidence relative risk (95% confidence interval) of 8.79(1.82-42.54) and 2.33(1.17-4.65), respectively.Conclusions: Our findings indicate that famine exposure in early life is an independent predictor on type 2 diabetes, particularly in women. The identification and intervention on critical time can prevent residents from diabetes in later life.The clinical trial was registered, more detail linked in https://clinicaltrials.gov/ct2/home, as registration no. NCT01053195.


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.


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