scholarly journals Does maternal overnutrition during pregnancy cause obesity in offspring?

2021 ◽  
Vol 19 (1) ◽  
pp. 62
Author(s):  
ChidiebereEmmanuel Okechukwu
Keyword(s):  
Maternal Overnutrition

scholarly journals Maternal Overnutrition Induces Long-Term Cognitive Deficits across Several Generations

Nutrients ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 7 ◽  
Author(s):  
Gitalee Sarker ◽  
Daria Peleg-Raibstein
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cognitive Deficits ◽  
Maternal Obesity ◽  
Cognitive Impairments ◽  
Long Term Effects ◽  
Ample Evidence ◽  
Increased Risk ◽  
Maternal Overnutrition

Ample evidence from epidemiological studies has linked maternal obesity with metabolic disorders such as obesity, cardiovascular disease, and diabetes in the next generation. Recently, it was also shown that maternal obesity has long-term effects on the progeny’s central nervous system. However, very little is known regarding how maternal overnutrition may affect, in particular, the cognitive abilities of the offspring. We reported that first-generation offspring exposed to a maternal high-fat diet (MHFD) displayed age-dependent cognitive deficits. These deficits were associated with attenuations of amino acid levels in the medial prefrontal cortex and the hippocampus regions of MHFD offspring. Here, we tested the hypothesis that MHFD in mice may induce long-term cognitive impairments and neurochemical dysfunctions in the second and third generations. We found that MHFD led to cognitive disabilities and an altered response to a noncompetitive receptor antagonist of the N-Methyl-D-aspartic acid (NMDA) receptor in adult MHFD offspring in both second and third generations in a sex-specific manner. Our results suggest that maternal overnutrition leads to an increased risk of developing obesity in subsequent generations as well as to cognitive impairments, affecting learning and memory processes in adulthood. Furthermore, MHFD exposure may facilitate pathological brain aging which is not a consequence of obesity. Our findings shed light on the long-term effects of maternal overnutrition on the development of the central nervous system and the underlying mechanisms which these traits relate to disease predisposition.

scholarly journals Maternal Obesity and Developmental Programming of Metabolic Disorders in Offspring: Evidence from Animal Models

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
M. Li ◽  
D. M. Sloboda ◽  
M. H. Vickers
Keyword(s):  
Animal Models ◽  
Early Life ◽  
Metabolic Disorders ◽  
Maternal Obesity ◽  
Maternal Weight ◽  
Critical Window ◽  
Obesity Epidemic ◽  
Obesity And Overweight ◽  
Increased Risk ◽  
Maternal Overnutrition

The incidence of obesity and overweight has reached epidemic proportions in the developed world as well as in those countries transitioning to first world economies, and this represents a major global health problem. Concern is rising over the rapid increases in childhood obesity and metabolic disease that will translate into later adult obesity. Although an obesogenic nutritional environment and increasingly sedentary lifestyle contribute to our risk of developing obesity, a growing body of evidence links early life nutritional adversity to the development of long-term metabolic disorders. In particular, the increasing prevalence of maternal obesity and excess maternal weight gain has been associated with a heightened risk of obesity development in offspring in addition to an increased risk of pregnancy-related complications. The mechanisms that link maternal obesity to obesity in offspring and the level of gene-environment interactions are not well understood, but the early life environment may represent a critical window for which intervention strategies could be developed to curb the current obesity epidemic. This paper will discuss the various animal models of maternal overnutrition and their importance in our understanding of the mechanisms underlying altered obesity risk in offspring.

1171-P: HORMAD1, a Novel Hypoxia-Inducible Factor-1 Target, Is Upregulated in Maternal Overnutrition-Induced Nonalcoholic Steatohepatitis (NASH)/Hepatocellular Carcinoma

Diabetes ◽  
2021 ◽  
Vol 70 (Supplement 1) ◽  
pp. 1171-P
Author(s):  
TAKAO TAKIYAMA ◽  
RYOICHI BESSHO ◽  
HIROYA KITSUNAI ◽  
YASUTAKA TAKEDA ◽  
HIDEMITSU SAKAGAMI ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Nonalcoholic Steatohepatitis ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1 ◽  
Maternal Overnutrition

scholarly journals Priming of Hypothalamic Ghrelin Signaling and Microglia Activation Exacerbate Feeding in Rats’ Offspring Following Maternal Overnutrition

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1241 ◽  
Author(s):  
Roger Maldonado-Ruiz ◽  
Marcela Cárdenas-Tueme ◽  
Larisa Montalvo-Martínez ◽  
Roman Vidaltamayo ◽  
Lourdes Garza-Ocañas ◽  
...  
Keyword(s):  
Food Intake ◽  
Palmitic Acid ◽  
Cell Activation ◽  
Programming Model ◽  
Microglia Activation ◽  
Tnf Alpha ◽  
Primary Microglia ◽  
Female Wistar Rats ◽  
C6 Ceramide ◽  
Maternal Overnutrition

Maternal overnutrition during pregnancy leads to metabolic alterations, including obesity, hyperphagia, and inflammation in the offspring. Nutritional priming of central inflammation and its role in ghrelin sensitivity during fed and fasted states have not been analyzed. The current study aims to identify the effect of maternal programming on microglia activation and ghrelin-induced activation of hypothalamic neurons leading to food intake response. We employed a nutritional programming model exposing female Wistar rats to a cafeteria diet (CAF) from pre-pregnancy to weaning. Food intake in male offspring was determined daily after fasting and subcutaneous injection of ghrelin. Hypothalamic ghrelin sensitivity and microglia activation was evaluated using immunodetection for Iba-1 and c-Fos markers, and Western blot for TBK1 signaling. Release of TNF-alpha, IL-6, and IL-1β after stimulation with palmitic, oleic, linoleic acid, or C6 ceramide in primary microglia culture were quantified using ELISA. We found that programmed offspring by CAF diet exhibits overfeeding after fasting and peripheral ghrelin administration, which correlates with an increase in the hypothalamic Iba-1 microglia marker and c-Fos cell activation. Additionally, in contrast to oleic, linoleic, or C6 ceramide stimulation in primary microglia culture, stimulation with palmitic acid for 24 h promotes TNF-alpha, IL-6, and IL-1β release and TBK1 activation. Notably, intracerebroventricular (i.c.v.) palmitic acid or LPS inoculation for five days promotes daily increase in food intake and food consumption after ghrelin administration. Finally, we found that i.c.v. palmitic acid substantially activates hypothalamic Iba-1 microglia marker and c-Fos. Together, our results suggest that maternal nutritional programing primes ghrelin sensitivity and microglia activation, which potentially might mirror hypothalamic administration of the saturated palmitic acid.

Maternal nutrition during pregnancy and health of the offspring

2006 ◽  
Vol 34 (5) ◽  
pp. 779-782 ◽  
Author(s):  
M.S. Martin-Gronert ◽  
S.E. Ozanne
Keyword(s):  
Animal Studies ◽  
Molecular Mechanisms ◽  
Maternal Nutrition ◽  
Critical Factor ◽  
The Body ◽  
Long Term Effects ◽  
Insulin Dependent ◽  
Fetal Malnutrition ◽  
And Function ◽  
Maternal Overnutrition

The ability of mother to provide nutrients and oxygen for her baby is a critical factor for fetal health and its survival. Failure in supplying the adequate amount of nutrients to meet fetal demand can lead to fetal malnutrition. The fetus responds and adapts to undernutrition but by doing so it permanently alters the structure and function of the body. Maternal overnutrition also has long-lasting and detrimental effects on the health of the offspring. There is growing evidence that maternal nutrition can induce epigenetic modifications of the fetal genome. Only relatively recently has evidence from epidemiological and animal studies emerged suggesting that fetal responses to the intrauterine environment may underlie the prevalence of many chronic diseases of adulthood including Type 2 (non-insulin-dependent) diabetes. It is now of crucial importance to gain the understanding of the molecular mechanisms underlying the relationship between fetal alterations to the intra-uterine environment and their long-term effects on the health of an individual.

Effect of maternal overnutrition on foal glucose and insulin dynamics and pancreatic development

2017 ◽  
Vol 52 ◽  
pp. 49
Author(s):  
A.N. Bradbery ◽  
J.A. Coverdale ◽  
C.J. Hartz ◽  
A.A. Millican ◽  
M.S. Goehring ◽  
...  
Keyword(s):  
Pancreatic Development ◽  
Maternal Overnutrition

Altered adipose tissue metabolism in offspring of dietary obese rat dams

2011 ◽  
Vol 121 (1) ◽  
pp. 19-28 ◽  
Author(s):  
Nassira Batoul Benkalfat ◽  
Hafida Merzouk ◽  
Samira Bouanane ◽  
Sid-Ahmed Merzouk ◽  
Jérôme Bellenger ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Unsaturated Fatty Acids ◽  
Cafeteria Diet ◽  
High Fat ◽  
Adipose Tissue Metabolism ◽  
Tissue Metabolism ◽  
Obese Rats ◽  
Maternal Overnutrition ◽  
The Impact

To investigate further the mechanisms of developmental programming, we analysed the effects of maternal overnutrition and of postnatal high-fat feeding on adipose tissue metabolism in the offspring. Postnatal changes in serum adiponectin, leptin and TAG [triacylglycerol (triglyceride)] levels, adipose tissue TAGs, fatty acids and enzyme activities were determined in offspring of cafeteria-diet-fed dams during gestation and lactation, weaned on to standard chow or on to cafeteria diet. Obese rats showed higher adiposity (+35% to 85%) as well as a significant increase in serum glucose, insulin, leptin, adiponectin and TAG levels (P<0.01) and adipose tissue LPL (lipoprotein lipase) and GPDH (glycerol-3-phosphate dehydrogenase) activities (P<0.01), compared with control pups at weaning (day 21) and at adulthood (day 90). Adipose HSL (hormone-sensitive lipase) activity was increased only at day 90 (P<0.05), and FAS (fatty acid synthase) activity remained unchanged. The proportions of SFAs (saturated fatty acids) and MUFAs (mono-unsaturated fatty acids) and the Δ9-desaturation index were significantly increased (P<0.05), whereas PUFAs (polyunsaturated fatty acids) were decreased (P<0.01) in serum and adipose TAGs of obese pups compared with controls. The cafeteria diet at weaning induced more severe abnormalities in obese rats. In conclusion, maternal overnutrition induced permanent changes in adipose tissue metabolism of the offspring. These pre-existing alterations in offspring were worsened under a high-fat diet from weaning to adulthood. Consequently, adipose adipokines and enzymes could provide a potential therapeutic target, and new investigations in this field could constitute strategies to improve the impact of early-life overnutrition.

Maternal overnutrition enhances mRNA expression of adipogenic markers and collagen deposition in skeletal muscle of beef cattle fetuses1

2014 ◽  
Vol 92 (9) ◽  
pp. 3846-3854 ◽  
Author(s):  
M. S. Duarte ◽  
M. P. Gionbelli ◽  
P. V. R. Paulino ◽  
N. V. L. Serão ◽  
C. S. Nascimento ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Beef Cattle ◽  
Mrna Expression ◽  
Collagen Deposition ◽  
Maternal Overnutrition
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