The association of early life socioeconomic conditions with prediabetes and type 2 diabetes: results from the Maastricht study

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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Associations between early-life food deprivation during World War II and risk of hypertension and type 2 diabetes at adulthood

Scientific Reports ◽

10.1038/s41598-020-62576-w ◽

2020 ◽

Vol 10 (1) ◽

Author(s):

Julia Mink ◽

Marie-Christine Boutron-Ruault ◽

Marie-Aline Charles ◽

Olivier Allais ◽

Guy Fagherazzi

Keyword(s):

Type 2 Diabetes ◽

World War Ii ◽

Food Deprivation ◽

Early Life ◽

World War

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Food contaminants and programming of type 2 diabetes: recent findings from animal studies

Journal of Developmental Origins of Health and Disease ◽

10.1017/s2040174416000210 ◽

2016 ◽

Vol 7 (5) ◽

pp. 505-512 ◽

Cited By ~ 5

Author(s):

S. Firmin ◽

N. Bahi-Jaber ◽

L. Abdennebi-Najar

Keyword(s):

Type 2 Diabetes ◽

Early Life ◽

Animal Studies ◽

Cell Mass ◽

Later Life ◽

Adult Health ◽

Food Contaminants ◽

Insulin Synthesis ◽

Increased Risk

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.

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Su1987 - Early Life Stress Induces type 2 Diabetes-Like Symptoms at Adulthood in Mice Associated with Defect of Intestinal Il17 and Il22 Secretion

Gastroenterology ◽

10.1016/s0016-5085(18)32333-3 ◽

2018 ◽

Vol 154 (6) ◽

pp. S-656-S-657

Author(s):

Hanna Ilchmann ◽

Maiwenn Olier ◽

Corinne Lencina ◽

Sandrine Ellero-Simatos ◽

Ambre Riba ◽

...

Keyword(s):

Type 2 Diabetes ◽

Life Stress ◽

Early Life ◽

Early Life Stress

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Early metabolic features of genetic liability to type 2 diabetes: cohort study with repeated metabolomics across early life

10.2337/figshare.12058923.v1 ◽

2020 ◽

Author(s):

Joshua A. Bell ◽

Caroline J. Bull ◽

Marc J. Gunter ◽

David Carslake ◽

Anubha Mahajan ◽

...

Keyword(s):

Type 2 Diabetes ◽

Amino Acids ◽

Early Life ◽

Genome Wide Association Study ◽

Genetic Risk Score ◽

Lipoprotein Subclass ◽

Adult Type ◽

Genetic Liability ◽

Branched Chain

Objective: Type 2 diabetes develops for many years before diagnosis. We aimed to reveal early metabolic features characterising liability to adult disease by examining genetic liability to adult type 2 diabetes in relation to metabolomic traits across early life. Research Design and Methods: <a>Up to 4,761 offspring from the Avon Longitudinal Study of Parents and Children</a> were studied. Linear models were used to examine effects of a genetic risk score (162 variants) for adult type 2 diabetes on 229 metabolomic traits (lipoprotein-subclass-specific cholesterol and triglycerides, amino acids, glycoprotein acetyls, others) measured at age 8y, 16y, 18y, and 25y. Two-sample Mendelian randomization (MR) was also conducted using genome-wide association study data on metabolomic traits in an independent sample of 24,925 adults. Results: At age 8y, associations were most evident for type 2 diabetes liability (per SD-higher) with lower lipids in high-density lipoprotein (HDL) subtypes, e.g. -0.03 SD (95% CI=-0.06, -0.003) for total lipids in very-large HDL. At 16y, associations were stronger with pre-glycemic traits including citrate and with glycoprotein acetyls (0.05 SD, 95% CI=0.01, 0.08), and at 18y, associations were stronger with branched chain amino acids. At 25y, associations had strengthened with VLDL lipids and remained consistent with previously altered traits including HDL lipids. Two-sample MR estimates among adults indicated persistent patterns of effect of disease liability. Conclusions: Our results support perturbed HDL lipid metabolism as one of the earliest features of <a>type 2 diabetes liability, alongside higher branched chain amino acid and inflammatory levels. Several features are apparent in childhood as early as age 8y, decades before the clinical onset of disease. </a>

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The ‘Jekyll and Hyde’ of Gluconeogenesis: Early-Life Adversity, Later Life Stress, and Metabolic Disturbances

10.20944/preprints202103.0090.v1 ◽

2021 ◽

Author(s):

Snehaa V. Seal ◽

Jonathan D. Turner

Keyword(s):

Type 2 Diabetes ◽

Energy Metabolism ◽

Hpa Axis ◽

Physiological Response ◽

Early Life ◽

Energy Homeostasis ◽

Early Life Adversity ◽

The Metabolic Syndrome ◽

Psychological Stressor

The physiological response to a psychological stressor broadly impacts energy metabolism. Inversely, changes in energy availability affect the physiological response to the stressor in terms of hypothalamus, pituitary adrenal gland axis and sympathetic nervous system activation upon exposure to a stressor. Glucocorticoids, the endpoint of the HPA axis, are critical checkpoints in endocrine control of energy homeostasis. Glucocorticoid actions have been linked to many severe metabolic diseases including obesity, insulin resistance and type 2 diabetes. Glucocorticoids, through the glucocorticoid receptor, activate transcription of many genes associated with glucose and lipid regulatory pathways and thereby intricately control both physiological and pathophysiological systemic energy homeostasis. Here, we summarize the current knowledge of glucocorticoid functions in energy metabolism and systemic metabolic dysfunction, particularly focusing on glucose and lipid metabolism. There are many elements in the external environment that induce lifelong changes in the HPA axis stress response and glucocorticoid levels, the most prominent are early-life adversity, or exposure to traumatic stress. We hypothesise that when the HPA axis is so disturbed after early-life adversity, it will fundamentally alter hepatic gluconeogenesis, inducing hyperglycaemia, and hence crystalise the significant lifelong risk of developing either the metabolic syndrome, or type 2 diabetes. This gives a “Jekyll and Hyde” role to gluconeogenesis, providing the necessary energy in situations of acute stress, but driving towards pathophysiological consequences when the HPA axis has been altered.

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Early Life Influences and Type-2 Diabetes – A Review

Current Science ◽

10.18520/cs/v113/i07/1311-1320 ◽

2017 ◽

Vol 113 (07) ◽

pp. 1311 ◽

Cited By ~ 2

Author(s):

Poornima Prabhakaran ◽

Nikhil Tandon

Keyword(s):

Type 2 Diabetes ◽

Early Life

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