scholarly journals Prenatal programming of postnatal obesity: fetal nutrition and the regulation of leptin synthesis and secretion before birth

2004 ◽  
Vol 63 (3) ◽  
pp. 405-412 ◽  
Author(s):  
I. C. McMillen ◽  
B. S. Muhlhausler ◽  
J. A. Duffield ◽  
B. S. J. Yuen
Keyword(s):  
Adipose Tissue ◽  
Fat Mass ◽  
Maternal Nutrition ◽  
Adult Life ◽  
Later Life ◽  
Late Gestation ◽  
Relative Mass ◽  
Moderate Increase ◽  
Fetal Life ◽  
Fat Depots

Exposure to either an increased or decreased level of intrauterine nutrition can result in an increase in adiposity and in circulating leptin concentrations in later life. In animals such as the sheep and pig in which fat is deposited before birth, leptin is synthesised in fetal adipose tissue and is present in the fetal circulation throughout late gestation. In the sheep a moderate increase or decrease in the level of maternal nutrition does not alter fetal plasma leptin concentrations, but there is evidence that chronic fetal hyperglycaemia and hyperinsulinaemia increase fetal fat mass and leptin synthesis within fetal fat depots. Importantly, there is a positive relationship between the relative mass of the ‘unilocular’ component of fetal perirenal and interscapular adipose tissue and circulating fetal leptin concentrations in the sheep. Thus, as in the neonate and adult, circulating leptin concentrations may be a signal of fat mass in fetal life. There is also evidence that leptin can act to regulate the lipid storage, leptin synthetic capacity and potential thermogenic functions of fat before birth. Thus, leptin may act as a signal of energy supply and have a ‘lipostatic’ role before birth. Future studies are clearly required to determine whether the intrauterine and early postnatal nutrient environment programme the endocrine feedback loop between adipose tissue and the central and peripheral neuroendocrine systems that regulate energy balance, resulting in an enhanced risk of obesity in adult life.

scholarly journals The role of adipokines in developmental programming: evidence from animal models

2019 ◽  
Vol 242 (1) ◽  
pp. T81-T94 ◽  
Author(s):  
Clare M Reynolds ◽  
Mark H Vickers
Keyword(s):  
Adipose Tissue ◽  
Animal Models ◽  
Maternal Nutrition ◽  
Adult Life ◽  
Empirical Support ◽  
Later Life ◽  
Developmental Programming ◽  
Critical Periods ◽  
Reproductive Disorders ◽  
Wide Range

Alterations in the environment during critical periods of development, including altered maternal nutrition, can increase the risk for the development of a range of metabolic, cardiovascular and reproductive disorders in offspring in adult life. Following the original epidemiological observations of David Barker that linked perturbed fetal growth to adult disease, a wide range of experimental animal models have provided empirical support for the developmental programming hypothesis. Although the mechanisms remain poorly defined, adipose tissue has been highlighted as playing a key role in the development of many disorders that manifest in later life. In particular, adipokines, including leptin and adiponectin, primarily secreted by adipose tissue, have now been shown to be important mediators of processes underpinning several phenotypic features associated with developmental programming including obesity, insulin sensitivity and reproductive disorders. Moreover, manipulation of adipokines in early life has provided for potential strategies to ameliorate or reverse the adverse sequalae that are associated with aberrant programming and provided insight into some of the mechanisms involved in the development of chronic disease across the lifecourse.

scholarly journals Endocrine and nutritional regulation of fetal adipose tissue development

2003 ◽  
Vol 179 (3) ◽  
pp. 293-299 ◽  
Author(s):  
ME Symonds ◽  
A Mostyn ◽  
S Pearce ◽  
H Budge ◽  
T Stephenson
Keyword(s):  
Adipose Tissue ◽  
Maternal Nutrition ◽  
Uncoupling Protein ◽  
Post Partum ◽  
Critical Role ◽  
Plasma Concentrations ◽  
Later Life ◽  
Postnatal Period ◽  
Late Gestation ◽  
Nutritional Regulation

In the fetus, adipose tIssue comprises both brown and white adipocytes for which brown fat is characterised as possessing the unique uncoupling protein (UCP)1. The dual characteristics of fetal fat reflect its critical role at birth in providing lipid that is mobilised rapidly following activation of UCP1 upon cold exposure to the extra-uterine environment. A key stage in the maturation of fetal fat is the gradual rise in the abundance of UCP1. For species with a mature hypothalamic-pituitary axis at birth there is a gradual increase in the amount and activity of UCP1 during late gestation, in conjunction with an increase in the plasma concentrations of catecholamines, thyroid hormones, cortisol, leptin and prolactin. These may act individually, or in combination, to promote UCP1 expression and, following the post-partum surge in each hormone, UCP1 abundance attains maximal amounts.Adipose tIssue grows in the fetus at a much lower rate than in the postnatal period. However, its growth is under marked nutritional constraints and, in contrast to many other fetal organs that are unaffected by nutritional manipulation, fat mass can be significantly altered by changes in maternal and, therefore, fetal nutrition. Fat deposition in the fetus is enhanced during late gestation following a previous period of nutrient restriction up to mid gestation. This is accompanied by increased mRNA abundance for the receptors of IGF-I and IGF-II. In contrast, increasing maternal nutrition in late gestation results in less adipose tIssue deposition but enhanced UCP1 abundance. The pronounced nutritional sensitivity of fetal adipose tIssue to both increased and decreased maternal nutrition may explain why the consequences of an adverse nutritional environment persist into later life.

scholarly journals Gestational Diabetes Mellitus and Infant Adiposity at Birth: A Systematic Review and Meta-Analysis of Therapeutic Interventions

2021 ◽  
Vol 10 (4) ◽  
pp. 835
Author(s):  
Manoja P. Herath ◽  
Jeffrey M. Beckett ◽  
Andrew P. Hills ◽  
Nuala M. Byrne ◽  
Kiran D. K. Ahuja
Keyword(s):  
Diabetes Mellitus ◽  
Adipose Tissue ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Fat Mass ◽  
Metabolic Disorders ◽  
Later Life ◽  
Therapeutic Interventions ◽  
Increased Risk ◽  
The Impact

Exposure to untreated gestational diabetes mellitus (GDM) in utero increases the risk of obesity and type 2 diabetes in adulthood, and increased adiposity in GDM-exposed infants is suggested as a plausible mediator of this increased risk of later-life metabolic disorders. Evidence is equivocal regarding the impact of good glycaemic control in GDM mothers on infant adiposity at birth. We systematically reviewed studies reporting fat mass (FM), percent fat mass (%FM) and skinfold thicknesses (SFT) at birth in infants of mothers with GDM controlled with therapeutic interventions (IGDMtr). While treating GDM lowered FM in newborns compared to no treatment, there was no difference in FM and SFT according to the type of treatment (insulin, metformin, glyburide). IGDMtr had higher overall adiposity (mean difference, 95% confidence interval) measured with FM (68.46 g, 29.91 to 107.01) and %FM (1.98%, 0.54 to 3.42) but similar subcutaneous adiposity measured with SFT, compared to infants exposed to normal glucose tolerance (INGT). This suggests that IGDMtr may be characterised by excess fat accrual in internal adipose tissue. Given that intra-abdominal adiposity is a major risk factor for metabolic disorders, future studies should distinguish adipose tissue distribution of IGDMtr and INGT.

The Diet of Girls and Young Women at the Beginning of the Century

1993 ◽  
Vol 9 (1) ◽  
pp. 15-23 ◽  
Author(s):  
J. Fellague Ariouat ◽  
D.J.P. Barker
Keyword(s):  
Cardiovascular Disease ◽  
Young Women ◽  
Cardiovascular Mortality ◽  
Maternal Nutrition ◽  
Adult Life ◽  
Cardiovascular Death ◽  
Early Growth ◽  
Fetal Life ◽  
Fertility Rates ◽  
Death Rates

Recent research has shown that retarded growth during fetal life and infancy is linked to the development of cardiovascular disease (coronary heart disease and stroke) in adult life. Maternal nutrition has an important effect on early growth and the diets of young women may therefore influence cardiovascular disease in the next generation. Samples of women aged 80 years and over were interviewed in six areas of England and Wales with different cardiovascular death rates. The women, 281 in total, were asked about their diets when they were aged 10 to 15 years. Those who grew up in areas which now have low cardiovascular mortality tended to eat four meals a day rather than three, to live in households which had gardens, kept hens or livestock, and to go into domestic service, where diets were generally good. Those who grew up in areas which now have high cardiovascular mortality tended to eat less red meat, to live in houses without gardens, to enter industrial occupations and have higher fertility rates.

scholarly journals Changes in adipose tissue physiology during the first two weeks posthatch in chicks from lines selected for low or high body weight

2019 ◽  
Vol 316 (6) ◽  
pp. R802-R818 ◽  
Author(s):  
Yang Xiao ◽  
Guoqing Wang ◽  
Miranda E. Gerrard ◽  
Sarah Wieland ◽  
Mary Davis ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Fat Mass ◽  
Peroxisome Proliferator ◽  
Adipocyte Size ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nonesterified Fatty Acids ◽  
Development Patterns ◽  
Fat Depots ◽  
Enhancer Binding Protein

Chickens from lines selected for low (LWS) or high (HWS) body weight (BW) differ in appetite and adiposity. Mechanisms associated with the predisposition to becoming obese are unclear. The objective of the experiment was to evaluate developmental changes in depot-specific adipose tissue during the first 2 wk posthatch. Subcutaneous (SQ), clavicular (CL), and abdominal (AB) depots were collected at hatch (DOH) and days 4 (D4) and 14 (D14) posthatch for histological and mRNA measurements. LWS chicks had decreased SQ fat mass on a BW basis with reduced adipocyte size from DOH to D4 and increased BW and fat mass with unchanged adipocyte size from D4 to D14. HWS chicks increased in BW from DOH to D14 and increased in fat mass in all three depots with enlarged adipocytes in the AB depot from D4 to D14. Meanwhile, CCAAT/enhancer-binding protein-α, neuropeptide Y, peroxisome proliferator-activated receptor-γ, and acyl-CoA dehydrogenase mRNAs differed among depots between lines at different ages. Plasma nonesterified fatty acids were greater in LWS than HWS at D4 and D14. From DOH to D4, LWS chicks mobilized SQ fat and replenished the reservoir through hyperplasia, whereas HWS chicks were dependent on hyperplasia and hypertrophy to maintain adipocyte size and depot mass. From D4 to D14, adipose tissue catabolism and adipogenesis slowed. Whereas LWS fat depots and adipocyte sizes remained stable, HWS chicks rapidly accumulated fat in CL and AB depots. Chicks predisposed to be anorexic or obese have different fat development patterns during the first 2 wk posthatch.

Fetal and neonatal adipose maturation: a primary site of cytokine and cytokine-receptor action

2001 ◽  
Vol 29 (2) ◽  
pp. 80-85 ◽  
Author(s):  
T. Stephenson ◽  
H. Budge ◽  
A. Mostyn ◽  
S. Pearce ◽  
R. Webb ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Maternal Nutrition ◽  
Short Form ◽  
Uncoupling Protein ◽  
Prolactin Receptor ◽  
Late Gestation ◽  
Metabolic Adaptation ◽  
Postnatal Life ◽  
Brown Adipose

During late gestation, the maturation of fetal adipose tissue is geared towards the synthesis of high levels of uncoupling protein 1 (UCP1), which is unique to brown adipose tissue. At birth, rapid activation of UCP1 ensures a large increase in heat production. These adaptations are nutritionally sensitive, and may be mediated in part by rapid changes in prolactin and leptin secretion after birth. Restriction of maternal nutrition reduces adipose tissue deposition, with no effect on UCP1. Increased maternal food intake results in increases in levels of UCP1 and the short form of the prolactin receptor, but in a decrease in adipose tissue content per kg of fetus. The ontogeny of the long and short forms of the prolactin receptor follows that of UCP1, to peak at birth. Then, during postnatal life, UCP1 disappears in parallel with the loss of prolactin receptors. Treatment of neonatal lambs with prolactin increases body temperature and the thermogenic potential of brown adipose tissue. In contrast, acute leptin treatment results in maintenance of colonic temperature, but chronic leptin treatment accelerates UCP1 loss. Increasing our understanding of the interaction between prolactin and leptin during perinatal development may enable the establishment of strategies aimed at maximizing adipose tissue development in order to promote metabolic adaptation to the extra-uterine environment.

Maternal Nutrition and Fetal Programming of the Immune System: Epidemiological and Experimental Evidences

2019 ◽  
pp. 1-8
Author(s):  
Siti Rohaiza Ahmad
Keyword(s):  
Immune System ◽  
Fetal Programming ◽  
Maternal Nutrition ◽  
Negative Impact ◽  
Experimental Studies ◽  
Adult Life ◽  
Experimental Models ◽  
Fetal Life ◽  
Immune Functions ◽  
Immune System Development

Maternal nutrition will not only affects pregnancy outcomes (such as birth weight) but will also affect the state of the fetus in their adult life in terms of diseases occurrence and also immune system development. Inadequate nutrition particularly will have a negative impact on the proliferation of the various cell populations responsible for the immune functions as well as the accumulation of high concentrations of inflammatory components. Maternal nutrition affects immunity ‘programming' during the period of pre-natal and post-natal life. Over the last decade, epidemiological and experimental studies have helped to expedite more understanding of immunity ‘programming.' External exposures such as smoking, alcohol and drugs during fetal life have also shown to have an impact on immunity ‘programming.' In this review, the relationship between fetal programming and the immune system, such as effects on the various immune-cellular components through some evidence from epidemiological and experimental models will be discussed.

Maternal and fetal lipid metabolism under normal and gestational diabetic conditions

2016 ◽  
Vol 26 (2) ◽  
Author(s):  
Emilio Herrera ◽  
Gernot Desoye
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Energy Production ◽  
Later Life ◽  
Fetal Tissue ◽  
Maternal Circulation ◽  
Fat Depots ◽  
Estrogen Effects ◽  
To Receive ◽  
Maternal Lipids

AbstractMaternal lipids are strong determinants of fetal fat mass. Here we review the overall lipid metabolism in normal and gestational diabetes mellitus (GDM) pregnancies. During early pregnancy, the increase in maternal fat depots is facilitated by insulin, followed by increased adipose tissue breakdown and subsequent hypertriglyceridemia, mainly as a result of insulin resistance (IR) and estrogen effects. The response to diabetes is variable as a result of greater IR but decreased estrogen levels. The vast majority of fatty acids (FAs) in the maternal circulation are esterified and associated with lipoproteins. These are taken up by the placenta and hydrolyzed by lipases. The released FAs enter various metabolic routes and are released into fetal circulation. Although these determinants are modified in maternal GDM, the fetus does not seem to receive more FAs than in non-GDM pregnancies. Long-chain polyunsaturated FAs are essential for fetal development and are obtained from the mother. Mitochondrial FA oxidation occurs in fetal tissue and in placenta and contributes to energy production. Fetal fat accretion during the last weeks of gestation occurs very rapidly and is sustained not only by FAs crossing the placenta, but also by fetal lipogenesis. Fetal hyperinsulinemia in GDM mothers promotes excess accretion of adipose tissue, which gives rise to altered adipocytokine profiles. Fetal lipoproteins are low at birth, but the GDM effects are unclear. The increase in body fat in neonates of GDM women is a risk factor for obesity in early childhood and later life.

scholarly journals Accelerated developmental adipogenesis programs adipose tissue dysfunction and cardiometabolic risk in offspring born to dams with metabolic dysfunction

2021 ◽  
Author(s):  
Anna Mikolajczak ◽  
Nada A Sallam ◽  
Radha D Singh ◽  
Taylor B Scheidl ◽  
Emma J. Walsh ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fat Mass ◽  
Cardiometabolic Risk ◽  
Late Gestation ◽  
Whole Body ◽  
Distribution Analysis ◽  
Metabolic Dysfunction ◽  
Wild Type ◽  
Cell Size Distribution ◽  
Differentiation Potential

This study determined if a perturbation in in utero adipogenesis leading to later-life adipose tissue (AT) dysfunction underlies programming of cardiometabolic risk in offspring born to dams with metabolic dysfunction. Female mice heterozygous for the leptin receptor deficiency (Hetdb) had 2.4-fold higher pre-pregnancy fat mass and in late gestation had higher plasma insulin and triglycerides, compared to wild-type (Wt) females (p < 0.05). To isolate the role of the intrauterine milieu, wild-type (Wt) offspring from each pregnancy were studied. Differentiation potential in isolated progenitors and cell size distribution analysis revealed accelerated adipogenesis in Wt pups born to Hetdb dams, accompanied by a higher accumulation of neonatal fat mass. In adulthood, whole-body fat mass by NMR was higher in male (69%) and female (20%) Wt offspring born to Hetdb vs. Wt pregnancies, along with adipocyte hypertrophy and hyperlipidemia (all p < 0.05). Lipidomic analyses by gas chromatography revealed an increased lipogenic index (16:0/18:2n6) after high fat/fructose diet (HFFD). Postprandial insulin, ADIPO-IR and ex vivo AT lipolytic responses to isoproterenol, were all higher in Wt offspring born to Hetdb dams (p < 0.05). Intrauterine metabolic stimuli may direct a greater proportion of progenitors toward terminal differentiation, thereby predisposing to hypertrophy-induced adipocyte dysfunction.

Sign in / Sign up

Export Citation Format

Share Document