scholarly journals The Effect and Potential Mechanism of Maternal Micronutrient Intake on Offspring Glucose Metabolism: An Emerging Field

2021 ◽  
Vol 8 ◽  
Author(s):  
Yifan Wu ◽  
Qian Zhang ◽  
Xinhua Xiao
Keyword(s):  
Glucose Metabolism ◽  
Early Life ◽  
Metabolic Diseases ◽  
Later Life ◽  
Underlying Mechanism ◽  
Early Life Environment ◽  
Micronutrient Status ◽  
Micronutrient Intake ◽  
Genetic And Environmental Factors

Diabetes has become the most common metabolic disease around the world. In addition to genetic and environmental factors in adulthood, the early life environment is critical to the progression of diabetes in adults, especially the environment during the fetal period; this concept is called “fetal programming.” Substantial evidence has illustrated the key role of early life macronutrient in programming metabolic diseases. Recently, the effect of maternal micronutrient intake on offspring glucose metabolism during later life has become an emerging field. This review focuses on updated human and animal evidence about the effect of maternal micronutrient status on offspring glucose metabolism and the underlying mechanism.

scholarly journals DNA methylation: the pivotal interaction between early-life nutrition and glucose metabolism in later life

2014 ◽  
Vol 112 (11) ◽  
pp. 1850-1857 ◽  
Author(s):  
Jia Zheng ◽  
Xinhua Xiao ◽  
Qian Zhang ◽  
Miao Yu
Keyword(s):  
Gene Expression ◽  
Glucose Metabolism ◽  
Early Life ◽  
Metabolic Diseases ◽  
Disease Risk ◽  
Critical Role ◽  
Critical Time ◽  
Later Life ◽  
Specific Gene ◽  
Obesity And Diabetes

Traditionally, it has been widely acknowledged that genes together with adult lifestyle factors determine the risk of developing some metabolic diseases such as insulin resistance, obesity and diabetes mellitus in later life. However, there is now substantial evidence that prenatal and early-postnatal nutrition play a critical role in determining susceptibility to these diseases in later life. Maternal nutrition has historically been a key determinant for offspring health, and gestation is the critical time window that can affect the growth and development of offspring. The Developmental Origins of Health and Disease (DOHaD) hypothesis proposes that exposures during early life play a critical role in determining the risk of developing metabolic diseases in adulthood. Currently, there are substantial epidemiological studies and experimental animal models that have demonstrated that nutritional disturbances during the critical periods of early-life development can significantly have an impact on the predisposition to developing some metabolic diseases in later life. The hypothesis that epigenetic mechanisms may link imbalanced early-life nutrition with altered disease risk has been widely accepted in recent years. Epigenetics can be defined as the study of heritable changes in gene expression that do not involve alterations in the DNA sequence. Epigenetic processes play a significant role in regulating tissue-specific gene expression, and hence alterations in these processes may induce long-term changes in gene function and metabolism that persist throughout the life course. The present review focuses on how nutrition in early life can alter the epigenome, produce different phenotypes and alter disease susceptibilities, especially for impaired glucose metabolism.

scholarly journals Role of small leucine zipper protein in hepatic gluconeogenesis and metabolic disorder

2020 ◽  
Author(s):  
Minsoo Kang ◽  
Sun Kyoung Han ◽  
Suhyun Kim ◽  
Sungyeon Park ◽  
Yerin Jo ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Glucose Metabolism ◽  
Metabolic Disorder ◽  
Leucine Zipper ◽  
Metabolic Diseases ◽  
Adenosine Monophosphate ◽  
The Body ◽  
Hepatic Gluconeogenesis ◽  
Leucine Zipper Protein

Abstract Hepatic gluconeogenesis is the central pathway for glucose generation in the body. The imbalance between glucose synthesis and uptake leads to metabolic diseases such as obesity, diabetes, and cardiovascular diseases. Small leucine zipper protein (sLZIP) is an isoform of LZIP and it mainly functions as a transcription factor. Although sLZIP is known to regulate the transcription of genes involved in various cellular processes, the role of sLZIP in hepatic glucose metabolism is not known. In this study, we investigated the regulatory role of sLZIP in hepatic gluconeogenesis and its involvement in metabolic disorder. We found that sLZIP expression was elevated during glucose starvation, leading to the promotion of phosphoenolpyruvate carboxylase and glucose-6-phosphatase expression in hepatocytes. However, sLZIP knockdown suppressed the expression of the gluconeogenic enzymes under low glucose conditions. sLZIP also enhanced glucose production in the human liver cells and mouse primary hepatic cells. Fasting-induced cyclic adenosine monophosphate impeded sLZIP degradation. Results of glucose and pyruvate tolerance tests showed that sLZIP transgenic mice exhibited abnormal blood glucose metabolism. These findings suggest that sLZIP is a novel regulator of gluconeogenic enzyme expression and plays a role in blood glucose homeostasis during starvation.

scholarly journals Epigenetics and DOHaD: from basics to birth and beyond

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
Keyword(s):  
Dna Methylation ◽  
Chronic Disease ◽  
Chronic Diseases ◽  
Early Life ◽  
Later Life ◽  
Metabolic Health ◽  
Number Of Children ◽  
Early Life Environment ◽  
Increased Risk ◽  
Early Life Exposures

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.

Predicting Health: The Role of the Early-Life Environment

2013 ◽  
pp. 266-295
Author(s):  
Luba Sominsky ◽  
Adam K. Walker ◽  
Deborah M. Hodgson
Keyword(s):  
Early Life ◽  
Early Life Environment

What role for the ‘long arm of childhood’ in social gradients in health? An international comparison of high-income contexts

2020 ◽  
Author(s):  
Steven A. Haas ◽  
Zhangjun Zhou ◽  
Katsuya Oi
Keyword(s):  
Life Course ◽  
Early Life ◽  
Economic Status ◽  
Functional Limitation ◽  
Later Life ◽  
High Income ◽  
Childhood Health ◽  
Relative Contribution ◽  
Early Life Factors

Social gradients in health have been a focus of research for decades. Two important lines of social gradient research have examined (1) international variation in their magnitude and (2) their life course / developmental antecedents. The present study brings these two strands together to explore the developmental origins of educational gradients in health. We leverage data spanning 14 high-income contexts from the Health and Retirement Study and its sisters in Europe. We find that early-life health and socio-economic status consistently attenuate educational gradients in multimorbidity and functional limitation. However, the relative contribution of early-life factors to gradients varies substantially across contexts. The results suggest that research on social gradients, and population health broadly, would benefit from the unique insights available from a conceptual and empirical approach that integrates comparative and life course perspectives.<br /><br />Key messages<br /><ul><li>The magnitude of educational gradients in later life health depend, in part, on childhood health and socioeconomic circumstances.</li><br /><li>The role of early life factors in educational gradients in health varies substantially across high income contexts.</li></ul>

scholarly journals Glucose-6 Phosphate, a Central Hub for Liver Carbohydrate Metabolism

Metabolites ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 282 ◽  
Author(s):  
Fabienne Rajas ◽  
Amandine Gautier-Stein ◽  
Gilles Mithieux
Keyword(s):  
Glucose Metabolism ◽  
Metabolic Diseases ◽  
De Novo ◽  
Glycogen Synthesis ◽  
Metabolic Reprogramming ◽  
De Novo Lipogenesis ◽  
Type I ◽  
Alcoholic Fatty Liver ◽  
Hexosamine Pathway

Cells efficiently adjust their metabolism according to the abundance of nutrients and energy. The ability to switch cellular metabolism between anabolic and catabolic processes is critical for cell growth. Glucose-6 phosphate is the first intermediate of glucose metabolism and plays a central role in the energy metabolism of the liver. It acts as a hub to metabolically connect glycolysis, the pentose phosphate pathway, glycogen synthesis, de novo lipogenesis, and the hexosamine pathway. In this review, we describe the metabolic fate of glucose-6 phosphate in a healthy liver and the metabolic reprogramming occurring in two pathologies characterized by a deregulation of glucose homeostasis, namely type 2 diabetes, which is characterized by fasting hyperglycemia; and glycogen storage disease type I, where patients develop severe hypoglycemia during short fasting periods. In these two conditions, dysfunction of glucose metabolism results in non-alcoholic fatty liver disease, which may possibly lead to the development of hepatic tumors. Moreover, we also emphasize the role of the transcription factor carbohydrate response element-binding protein (ChREBP), known to link glucose and lipid metabolisms. In this regard, comparing these two metabolic diseases is a fruitful approach to better understand the key role of glucose-6 phosphate in liver metabolism in health and disease.

scholarly journals The Role of the Early-Life Environment in the Development of Allergic Disease

2015 ◽  
Vol 35 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Ganesa Wegienka ◽  
Edward Zoratti ◽  
Christine Cole Johnson
Keyword(s):  
Allergic Disease ◽  
Early Life ◽  
Early Life Environment

scholarly journals Intestinal microbiota during early life – impact on health and disease

2014 ◽  
Vol 73 (4) ◽  
pp. 457-469 ◽  
Author(s):  
Lotta Nylund ◽  
Reetta Satokari ◽  
Seppo Salminen ◽  
Willem M. de Vos
Keyword(s):  
Intestinal Microbiota ◽  
Early Life ◽  
Later Life ◽  
Related Factors ◽  
Life Impact ◽  
Health And Disease ◽  
And Function ◽  
The Impact

In the first years after birth, the intestinal microbiota develops rapidly both in diversity and complexity while being relatively stable in healthy adults. Different life-style-related factors as well as medical practices have an influence on the early-life intestinal colonisation. We address the impact of some of these factors on the consecutive microbiota development and later health. An overview is presented of the microbial colonisation steps and the role of the host in that process. Moreover, new early biomarkers are discussed with examples that include the association of microbiota and atopic diseases, the correlation of colic and early development and the impact of the use of antibiotics in early life. Our understanding of the development and function of the intestinal microbiota is constantly improving but the long-term influence of early-life microbiota on later life health deserves careful clinical studies.

Nuclear receptor PXR targets AKR1B7 to protect mitochondrial metabolism and renal function in AKI

2020 ◽  
Vol 12 (543) ◽  
pp. eaay7591 ◽  
Author(s):  
Xiaowen Yu ◽  
Man Xu ◽  
Xia Meng ◽  
Shumin Li ◽  
Qianqi Liu ◽  
...  
Keyword(s):  
Metabolic Diseases ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Public Health Problem ◽  
Pregnane X Receptor ◽  
Underlying Mechanism ◽  
Mitochondrial Metabolism ◽  
Luciferase Reporter ◽  
Proteomics Data

Acute kidney injury (AKI) is a worldwide public health problem with no specific and satisfactory therapies in clinic. The nuclear pregnane X receptor (PXR) is involved in the progression of multiple diseases, including metabolic diseases, atherosclerosis, hypertension, liver injury, etc. However, its role in kidney injury remains to be understood. In this study, we have investigated the role of PXR in AKI and underlying mechanism(s) involved in its function. PXR was robustly down-regulated and negatively correlated with renal dysfunction in human and animal kidneys with AKI. Silencing PXR in rats enhanced cisplatin-induced AKI and induced severe mitochondrial abnormalities, whereas activating PXR protected against AKI. Using luciferase reporter assays, genomic manipulation, and proteomics data analysis on the kidneys of PXR−/− rats, we determined that PXR targeted Aldo-keto reductase family 1, member B7 (AKR1B7) to improve mitochondrial function, thereby ameliorating AKI. We confirmed the protective role of PXR against kidney injury using genomic and pharmacologic approaches in an ischemia/reperfusion model of AKI. These findings demonstrate that disabling the PXR/AKR1B7/mitochondrial metabolism axis is an important factor that can contribute to AKI, whereas reestablishing this axis can be useful for treating AKI.

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