The influence of obesity and gestational diabetes mellitus on accretion and the distribution of adipose tissue in pregnancy

Ehrenberg, Hugh M.; Huston-Presley, Larraine; Catalano, Patrick M.

doi:10.1067/s0002-9378(03)00761-0

Cited by 110 publications

(85 citation statements)

References 18 publications

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“…This should allow drawing conclusions from the present results to effects of diabetes in human pregnancies, however, with the precautions that always have to be made when using animal models for human disease (5,36,37). One of the differences is that human offspring are born with 12-15% fat at term of pregnancy and in maternal diabetes, fetus and newborn are characterized by an excessive i.e., over proportional, accumulation of fat (18,37). Rodent fetuses are born with only about 2% fat, without mature adipocyte differentiation, making extrapolations about diabetes-induced differentiated adipose tissue accumulation impossible.…”

Section: Discussionmentioning

confidence: 99%

Diabetes-associated changes in the fetal insulin/insulin-like growth factor system are organ specific in rats

et al. 2014

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Background: Diabetes in pregnancy affects fetal growth and development. The insulin/insulin-like growth factors (IGF) system comprising insulin, IGF, their receptors, and binding proteins, has been implicated in fetal growth regulation. This study tested the hypothesis that maternal diabetes alters the fetal insulin/IGF system in a tissue-specific manner. Methods: Wistar rats were rendered diabetic by neonatal administration of streptozotocin and mated with control rats. At day 21 of gestation, the weights of fetuses, placentas, and fetal organs (heart, lung, liver, stomach, intestine, and pancreas) were determined. Maternal and fetal plasma concentrations of insulin, IGF1, and IGF2 were measured by ELISA, and expression of IGF1, IGF2, IGF1R, IGF2R, IR, IGFBP1, BP2, and BP3 in placenta and fetal organs by qPCR. results: The well-known increase in fetal growth in this model of mild diabetes is accompanied by elevated insulin and IGF1 levels and alterations of the insulin/IGF system in the fetus and the placenta. These alterations were organ and gene specific. The insulin/IGF system was generally upregulated, especially in the fetal heart, while it was downregulated in fetal lung. conclusion: In our model of mild diabetes, the effect of maternal diabetes on fetal weight and fetal insulin/IGF system expression is organ specific with highly sensitive organs such as lung and heart, and organs that were less affected, such as stomach. d iabetes in pregnancy, i.e., the fetal exposure to hyperglycemia in utero, has become recognized as a risk factor for immediate adverse pregnancy outcome, and in having longterm effects on mother and offspring. Immediate outcomes include excessive fetal fat accretion as well as congenital malformations, such as cardiac, musco-skeletal, and central nervous system anomalies (1,2). Early evidence in Pima Indians and in animal models has clearly shown that long-term effects of growing in a diabetic environment in utero include a higher risk for the offspring to develop obesity, type 2 diabetes (T2D), the metabolic syndrome, and cardiovascular disease later in life (3). This was confirmed in further studies in which offspring from diabetic pregnancies were followed up into adolescence (4).One of the well-known effects of the diabetic environment on the offspring is its growth promoting action as reflected by weight increases of the fetus proper and of some fetal tissues (5,6). The insulin/IGF system is a potent regulator of development and growth, and elevated levels of cord blood insulin can be regarded as hallmark of fetal changes in the wake of maternal diabetes (7,8). This system comprises insulin, the insulin-like growth factors-1 (IGF1) and -2 (IGF2), the receptors for insulin (IR), IGF1 (IGF1R) and IGF2 (IGF2R) as well as a range of binding proteins (IGFBP1-6) for both IGFs, which regulate IGF bioavailability by modulating the half-life of IGFs and their site of action (9). Only a small proportion of IGFs circulates in a free form, the bulk is bound to IGFbinding proteins (IGFBPs). Am...

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Section: Discussionmentioning

confidence: 99%

Diabetes-associated changes in the fetal insulin/insulin-like growth factor system are organ specific in rats

et al. 2014

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“…44,51 In women of healthy pre-pregnancy BMI, early gestational adipose tissue gains are laid down in the subcutaneous compartments of the breast, trunk and upper thigh, and during later pregnancy a small quantity of fat is stored as visceral adipose tissue. 52,53 Although there is conflict in published data, greater gain in gestational adiposity probably occurs in mothers who are overweight or obese prior to conception. Excess gestational fat in obese mothers is stored predominantly in the visceral compartment rather than in the subcutaneous compartments.…”

Section: Mechanisms Of Adverse Pregnancy Outcome In Obesitymentioning

confidence: 99%

“…Excess gestational fat in obese mothers is stored predominantly in the visceral compartment rather than in the subcutaneous compartments. 53,54 In the non-pregnant state, regional preference for visceral adiposity contributes to insulin resistance and metabolic complications of obesity. 55 The predisposition for gestational storage of excess visceral fat in obese and overweight mothers is likely to play a role in the pathogenesis of the homeostatic imbalance which characterizes the obese pregnancy, as visceral adiposity during pregnancy is associated with a higher risk of GDM and gestational hypertension/PET.…”

Section: Mechanisms Of Adverse Pregnancy Outcome In Obesitymentioning

confidence: 99%

The maternal and fetal impacts of obesity and gestational diabetes on pregnancy outcome

Dennedy

Dunne

2010

Best Practice & Research Clinical Endocrinology & Metab

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“…However, in these experiments the animals were fed a fat-rich diet during gestation/lactation but not before pregnancy. Pregnant mothers were therefore not overweight and did not display metabolic disturbances that were capable of interfering with fetal/postnatal programming (7). These data, therefore, only partly reflect the features of MetS.…”

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confidence: 99%

Resistance to high-fat diet in the female progeny of obese mice fed a control diet during the periconceptual, gestation, and lactation periods

Gallou-Kabani

Vigé²,

Gross³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Gallou-Kabani C, Vigé A, Gross M-S, Boileau C, Rabes J-P, Fruchart-Najib J, Jais J-P, Junien C. Resistance to high-fat diet in the female progeny of obese mice fed a control diet during the periconceptual, gestation, and lactation periods. Am J Physiol Endocrinol Metab 292: E1095-E1100, 2007. First published December 12, 2006; doi:10.1152/ajpendo.00390.2006.-With the worldwide epidemic of metabolic syndrome (MetS), the proportion of women that are overweight/obese and overfed during pregnancy has increased. The resulting abnormal uterine environment may have deleterious effects on fetal metabolic programming and lead to MetS in adulthood. A balanced/restricted diet and/or physical exercise often improve metabolic abnormalities in individuals with obesity and type 2 diabetes mellitus (T2D). We investigated whether reducing fat intake during the periconceptual/gestation/lactation period in mothers with high-fat diet (HFD)-induced obesity could be used to modify fetal/ neonatal MetS programming positively, thereby preventing MetS. First generation (F1) C57BL/6J female mice with HFD-induced obesity and T2D were crossed with F1 males on control diet (CD). These F1 females were switched to a CD during the periconceptual/ gestation/lactation period. At weaning, both male and female second generation (F2) mice were fed a HFD. Weight, caloric intake, lipid parameters, glucose, and insulin sensitivity were assessed. Sensitivity/ resistance to the HFD differed significantly between generations and sexes. A similar proportion of the F1 and F2 males (80%) developed hyperphagia, obesity, and T2D. In contrast, a significantly higher proportion of the F2 females (43%) than of the previous F1 generation (17%) were resistant (P Ͻ 0.01). Despite having free access to the HFD, these female mice were no longer hyperphagic and remained lean, with normal insulin sensitivity and glycemia but mild hypercholesterolemia and glucose intolerance, thus displaying a "satiety phenotype." This suggests that an appropriate dietary fatty acid profile and intake during the periconceptual/gestation/lactation period helps the female offspring to cope with deleterious intrauterine conditions. epigenetics; nutrition; metabolic syndrome; fetal programming THE WORLDWIDE EPIDEMIC of metabolic syndrome (MetS), combining disturbances in glucose and insulin metabolism, excess weight distributed predominantly around the abdomen, mild dyslipidemia, and hypertension, leading to obesity, type 2 diabetes mellitus (T2D), and cardiovascular disease, has become a major health concern (6). Like obesity and T2D, MetS is occurring earlier in childhood and worsening from generation to generation. It has been estimated that ϳ24% of US adults now present MetS (6). An increasing number of women are overweight and consuming a calorific or fat-rich diet before and during pregnancy and lactation. Human epidemiological studies and appropriate dietary interventions in animal models (3) have provided evidence to suggest that maternal nutritional imbalance and metabolic disturb...

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The influence of obesity and gestational diabetes mellitus on accretion and the distribution of adipose tissue in pregnancy

Cited by 110 publications

References 18 publications

Diabetes-associated changes in the fetal insulin/insulin-like growth factor system are organ specific in rats

Diabetes-associated changes in the fetal insulin/insulin-like growth factor system are organ specific in rats

The maternal and fetal impacts of obesity and gestational diabetes on pregnancy outcome

Resistance to high-fat diet in the female progeny of obese mice fed a control diet during the periconceptual, gestation, and lactation periods

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