Abstract:In early life, over-nutrition may increase the risk of insulin resistance in the adult stage. Adiponectin and its receptor may play a key role in this process. This study aimed to identify the effect of a high-fat (HF) maternal diet on metabolic parameters and muscle adiponectin signaling in young adult offspring. We found that offspring born to dams fed HF chow (HF; 31% of calories from fat) had elevated body and adipose tissue weight and higher serum glucose levels after glucose challenge at three weeks (W3)… Show more
“…99
SDM
na
63YASBPZaborska K.E. 101
SDM
na
na
YAFAT, INSHou M.SDM
na
56PPPFAT, GLU, INS, TGSome studies appear more than one time with different sex, age stage or timing of the intervention. Some of the studies reported more than one experiment and therefore sometimes more than one experimental group could be identified for the purposes of our analysis.…”
Section: Resultsmentioning
confidence: 99%
“…The initial screen was based on the paper’s title, abstract and occasional whole-text scan and then after in-depth screening, 203 relevant citations remained for further review. Finally, 68 citations were used in meta-analysis 13–17, 19–21, 23, 26, 38, 43, 44, 47–101 . The 135 excluded studies with the reasons for their exclusion are available in Supplementary Table S6.Figure 10PRISMA flow chart summarizing study selection processes.
…”
Numerous rodent studies have evaluated the effects of a maternal high-fat diet (HFD) on later in life susceptibility to Metabolic Syndrome (MetS) with varying results. Our aim was to quantitatively synthesize the available data on effects of maternal HFD around gestation on offspring’s body mass, body fat, plasma leptin, glucose, insulin, lipids and systolic blood pressure (SBP). Literature was screened and summary estimates of the effect of maternal HFD on outcomes were calculated by using fixed- or random-effects models. 362 effect sizes from 68 studies together with relevant moderators were collected. We found that maternal HFD is statistically associated with higher body fat, body weight, leptin, glucose, insulin and triglycerides levels, together with increased SBP in offspring later in life. Our analysis also revealed non-significant overall effect on offspring’s HDL-cholesterol. A main source of variation among studies emerged from rat strain and lard-based diet type. Strain and sex -specific effects on particular data subsets were detected. Recommendations are suggested for future research in the field of developmental programming of the MetS. Despite significant heterogeneity, our meta-analysis confirms that maternal HFD had long-term metabolic effects in offspring.
“…99
SDM
na
63YASBPZaborska K.E. 101
SDM
na
na
YAFAT, INSHou M.SDM
na
56PPPFAT, GLU, INS, TGSome studies appear more than one time with different sex, age stage or timing of the intervention. Some of the studies reported more than one experiment and therefore sometimes more than one experimental group could be identified for the purposes of our analysis.…”
Section: Resultsmentioning
confidence: 99%
“…The initial screen was based on the paper’s title, abstract and occasional whole-text scan and then after in-depth screening, 203 relevant citations remained for further review. Finally, 68 citations were used in meta-analysis 13–17, 19–21, 23, 26, 38, 43, 44, 47–101 . The 135 excluded studies with the reasons for their exclusion are available in Supplementary Table S6.Figure 10PRISMA flow chart summarizing study selection processes.
…”
Numerous rodent studies have evaluated the effects of a maternal high-fat diet (HFD) on later in life susceptibility to Metabolic Syndrome (MetS) with varying results. Our aim was to quantitatively synthesize the available data on effects of maternal HFD around gestation on offspring’s body mass, body fat, plasma leptin, glucose, insulin, lipids and systolic blood pressure (SBP). Literature was screened and summary estimates of the effect of maternal HFD on outcomes were calculated by using fixed- or random-effects models. 362 effect sizes from 68 studies together with relevant moderators were collected. We found that maternal HFD is statistically associated with higher body fat, body weight, leptin, glucose, insulin and triglycerides levels, together with increased SBP in offspring later in life. Our analysis also revealed non-significant overall effect on offspring’s HDL-cholesterol. A main source of variation among studies emerged from rat strain and lard-based diet type. Strain and sex -specific effects on particular data subsets were detected. Recommendations are suggested for future research in the field of developmental programming of the MetS. Despite significant heterogeneity, our meta-analysis confirms that maternal HFD had long-term metabolic effects in offspring.
“…Offspring of mothers fed high-fat diets grew to be significantly heavier and had significantly elevated fasting glucose levels compared to mice exposed to a normal maternal diet. 33 Given that ADIPOQ helps to maintain insulin sensitivity and ADIPOQ levels are inversely correlated with obesity, the results of this study suggest that metabolic disturbances in response to maternal high-fat diet may also be mediated by ADIPOQ. 33 …”
Section: Maternal and Early Postnatal Dietmentioning
confidence: 72%
“… 33 Given that ADIPOQ helps to maintain insulin sensitivity and ADIPOQ levels are inversely correlated with obesity, the results of this study suggest that metabolic disturbances in response to maternal high-fat diet may also be mediated by ADIPOQ. 33 …”
Section: Maternal and Early Postnatal Dietmentioning
Metabolic syndrome is a growing cause of morbidity and mortality worldwide. Metabolic syndrome is characterized by the presence of a variety of metabolic disturbances including obesity, hyperlipidemia, hypertension, and elevated fasting blood sugar. Although the risk for metabolic syndrome has largely been attributed to adult lifestyle factors such as poor nutrition, lack of exercise, and smoking, there is now strong evidence suggesting that predisposition to the development of metabolic syndrome begins in utero. First posited by Hales and Barker in 1992, the “thrifty phenotype” hypothesis proposes that susceptibility to adult chronic diseases can occur in response to exposures in the prenatal and perinatal periods. This hypothesis has been continually supported by epidemiologic studies and studies involving animal models. In this review, we describe the structural, metabolic and epigenetic changes that occur in response to adverse intrauterine environments including prenatal and postnatal diet, maternal obesity, and pregnancy complications. Given the increasing prevalence of metabolic syndrome in both the developed and developing worlds, a greater understanding and appreciation for the role of the intrauterine environment in adult chronic disease etiology is imperative.
“…Дети матерей, употреблявших большое количество жиров во время беременности, склонны к набору лишнего веса. Считается, что в этом случае дефицит адипонектина (гормона, ответственного за чувствительность к инсулину) является фактором, инициирующим эпигенетические модификации [33]. Диета с высоким содержанием жиров во время беременности инициирует недостаточную сосудорасширяющую реакцию на ацетилхолин у потомства.…”
The review article presents data on the effects of obesity on the female reproductive system and offspring of mothers with overweight or obesity, such as infertility, miscarriages, premature birth, stillbirth, congenital anomalies and prematurity, as well as a high risk of cesarean section. Obesity accompanies polycystic ovary syndrome, worsening the metabolic profile and increasing the risk of developing depression and eating disorders. Maternal obesity and hyperglycemia are able to influence the formation of the fetus by epigenetic mechanisms without affecting the nucleotide sequences. Subsequently, the metabolic and cardiovascular risks increase in the descendants of obese or overweight mothers and gestational diabetes. Patients with obesity are characterized by a folic acid deficiency and a deficiency of the luteal phase. Exogenous administration of these substances improves pregnancy outcomes and prevents congenital malformations.
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