Fetal life malnutrition was not reflected in the relative abundances of adiponectin and leptin mRNAs in adipose tissue in male mink kits at 9.5 weeks of age

Iodothyronine 5'-deiodinase activity appears to be a type I enzyme in bovine brown adipose tissue, on the basis of its high Km for 3,3',5'-tri-iodothyronine (‘reverse T3’) (in the micromolar range) and sensitivity to propylthiouracil inhibition. This enzyme activity is already detectable in perirenal adipose tissue of bovine fetuses in the second month of gestation, reaches peak values around the seventh month of fetal life, declines before birth, becomes lower after parturition and finally undetectable in the adult cow. Iodothyronine 5'-deiodinase activity is present in the pericardic, peritoneal and intermuscular adipose depots of the neonatal calf, but it is always undetectable in the subcutaneous adipose tissue. It is concluded that iodothyronine 5'-deiodinase is a specific feature of brown fat in the bovine species that is not shared by white adipose tissue. white adipose tissue. Peak values of 5'-deiodinating activity appear as an early event in the prenatal differentiation programme of bovine brown-fat cells as they occur when uncoupling-protein-gene expression first starts.

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Effect of the linoleic acid concentration of mother's diet on adenyl cyclase activity of fetal and neonatal rat brown adipose tissue

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y77-169 ◽

1977 ◽

Vol 55 (6) ◽

pp. 1242-1245 ◽

Cited By ~ 1

Author(s):

Thierry Cresteil

Keyword(s):

Adipose Tissue ◽

Linoleic Acid ◽

Brown Adipose Tissue ◽

Adenyl Cyclase ◽

Neonatal Rat ◽

Cyclase Activity ◽

Fetal Life ◽

Adenyl Cyclase Activity ◽

High Linoleic Acid ◽

Brown Adipose

An adenyl cyclase activity was measurable in the brown adipose tissue of fetal rat, and could be stimulated in vitro by noradrenaline during the last 3 days of fetal life. The stimulating effect of noradrenaline was maximal at birth and decreased during the first days of extrauterine life.Ingestion by mothers of a high lipid diet modified the developmental pattern of fetal adenyl cyclase. The linoleic acid content of mother's diet had no effect on the noradrenaline- or fluoride-stimulated specific activities except on the day 22 of gestation. Relative noradrenaline-stimulated activity, expressed as a fraction of the maximal activity, was significantly increased in fetuses and 1-day-old newborns from mothers fed a high linoleic acid diet, but no effect was observed in suckling newborns.

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Thyroid hormones and 5'-deiodinase in rat brown adipose tissue during fetal life

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1989.257.5.e625 ◽

1989 ◽

Vol 257 (5) ◽

pp. E625-E631 ◽

Cited By ~ 6

Author(s):

M. J. Obregon ◽

C. Ruiz de Ona ◽

A. Hernandez ◽

R. Calvo ◽

F. Escobar del Rey ◽

...

Keyword(s):

Adipose Tissue ◽

Thyroid Hormones ◽

Brown Adipose Tissue ◽

Marked Decrease ◽

Relative Weight ◽

Fetal Life ◽

Fetal Plasma ◽

Brown Adipose ◽

High Concentrations ◽

Very High

Brown adipose tissue (BAT) iodothyronine 5'-deiodinase (5'D) activities are very high during fetal life but decrease 10-fold a few hours before birth. Accordingly, BAT 3,5,3'-triiodothyronine (T3) concentrations are also very high. The temporal patterns of changes in BAT 5'-D and fetal plasma insulin are similar (and differ from the pattern for catecholamines) but are not superimposable. A causal role for insulin in the activation of fetal BAT 5'-D is therefore not supported by the data. Maternal thyroidectomy leads to a decrease in the total and relative weight of fetal BAT and to a 30-50% increase in BAT 5'-D activities; BAT thyroid hormone concentrations are essentially unchanged. Fetal hypothyroidism was induced by giving methimazole and resulted in a marked decrease of BAT thyroxine (T4) and T3 concentrations. This treatment increased BAT 5'-D activity only on day 21 of gestation, but no effect was observed on day 20. The fetal 5'-D response to thyroid hormones infused into the methimazole-treated dams was studied at 21 days of gestation. The increase in BAT 5'-D induced by methimazole treatment was prevented by T4 infused into control dams but not by T3. In fetuses from thyroidectomized dams, the pattern of 5'-D regulation by thyroid hormones was impaired. It is suggested that the high concentrations of thyroid hormones present in fetal BAT might participate in the general maturation and development of fetal BAT.

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Forced catch-up growth after fetal protein restriction alters the adipose tissue gene expression program leading to obesity in adult mice

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.90497.2008 ◽

2009 ◽

Vol 297 (2) ◽

pp. R291-R299 ◽

Cited By ~ 90

Author(s):

V. V. Bol ◽

A-I. Delattre ◽

B. Reusens ◽

M. Raes ◽

C. Remacle

Keyword(s):

Gene Expression ◽

Adipose Tissue ◽

Expression Profile ◽

Protein Restriction ◽

Fetal Life ◽

Male Mice ◽

Adipose Tissue Gene Expression ◽

Postnatal Environment ◽

Catch Up ◽

Tissue Gene Expression

A mismatch between fetal and postnatal environment can permanently alter the body structure and physiology and therefore contribute later to obesity and related disorders, as revealed by epidemiological studies. Early programming of adipose tissue might be central in this observation. Moreover, adipose tissue secretes adipokines that provide a molecular link between obesity and its related disorders. Therefore, our aim was to investigate whether a protein restriction during fetal life, followed by catch-up growth could lead to obesity in 9-mo-old male mice and could alter the adipose tissue gene expression profile. Dams were fed a low-protein (LP) or an isocaloric control (C) diet during gestation. Postnatal catch-up growth was induced in LP offspring by feeding dams with control diet and by culling LP litters to four pups instead of eight in the C group. At weaning, male mice were fed by lab chow alone (C) or supplemented with a hypercaloric diet (HC), to induce obesity (C-C, C-HC, LP-C, and LP-HC groups). At 9 mo, LP offspring featured increased relative fat mass, hyperglycemia, hypercholesterolemia, and hyperleptinemia. Using a microarray designed to study the expression of 89 genes involved in adipose tissue differentiation/function, we demonstrated that the expression profile of several genes were dependent upon the maternal diet. Among the diverse genes showing altered expression, we could identify genes encoding several enzymes involved in lipid metabolism. These results indicated that offspring submitted to early mismatched nutrition exhibited alterations in adipose tissue gene expression that probably increases their susceptibility to overweight when challenged after weaning with a HC diet.

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CCAAT/enhancer-binding proteins α and β in brown adipose tissue: evidence for a tissue-specific pattern of expression during development

Biochemical Journal ◽

10.1042/bj3020695 ◽

1994 ◽

Vol 302 (3) ◽

pp. 695-700 ◽

Cited By ~ 27

Author(s):

C Manchado ◽

P Yubero ◽

O Viñas ◽

R Iglesias ◽

F Villarroya ◽

...

Keyword(s):

Adipose Tissue ◽

Brown Adipose Tissue ◽

Uncoupling Protein ◽

Brown Fat ◽

Brown Adipocyte ◽

Fetal Life ◽

Inhibitory Protein ◽

Adult Rats ◽

Stage Of Development ◽

Brown Adipose

CCAAT/enhancer-binding protein (C/EBP) alpha mRNA and its protein products C/EBP alpha and 30 kDa C/EBP alpha are expressed in rat brown-adipose tissue. Results also demonstrate the expression of C/EBP beta mRNA and its protein products C/EBP beta and liver inhibitory protein (LIP) in the tissue. The abundance of C/EBP alpha and C/EBP beta proteins in adult brown fat is similar to that found in adult liver. However, the expression of C/EBP alpha and C/EBP beta is specifically regulated in brown fat during development. C/EBP alpha, 30 kDa C/EBP alpha, C/EBP beta and LIP content is several-fold higher in fetal brown fat than in the adult tissue, or liver at any stage of development. Peak values are attained in late fetal life, in concurrence with the onset of transcription of the uncoupling protein (UCP) gene, the molecular marker of terminal brown-adipocyte differentiation. When adult rats are exposed to a cold environment, which is a physiological stimulus of brown-adipose tissue hyperplasia and UCP gene expression, a specific rise in C/EBP beta expression with respect to C/EBP alpha, 30 kDa C/EBP alpha and LIP is observed. Present data suggest that the C/EBP family of transcription factors has an important role in the development and terminal differentiation of brown-adipose tissue.

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

Proceedings of The Nutrition Society ◽

10.1079/pns2004370 ◽

2004 ◽

Vol 63 (3) ◽

pp. 405-412 ◽

Cited By ~ 80

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.

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Developmental programming: interaction between prenatal BPA exposure and postnatal adiposity on metabolic variables in female sheep

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00425.2015 ◽

2016 ◽

Vol 310 (3) ◽

pp. E238-E247 ◽

Cited By ~ 23

Author(s):

Almudena Veiga-Lopez ◽

Jacob Moeller ◽

Rohit Sreedharan ◽

Kanakadurga Singer ◽

Carey Lumeng ◽

...

Keyword(s):

Insulin Resistance ◽

Adipose Tissue ◽

Cohort Study ◽

Visceral Fat ◽

Subcutaneous Fat ◽

Consumer Products ◽

Fetal Life ◽

Metabolic Outcomes ◽

Adipocyte Hypertrophy ◽

Fat Depot

Among potential contributors for the increased incidence of metabolic diseases is the developmental exposure to endocrine-disrupting chemicals such as bisphenol A (BPA). BPA is an estrogenic chemical used in a variety of consumer products. Evidence points to interactions of BPA with the prevailing environment. The aim of this study was to assess the effects of prenatal exposure to BPA on postnatal metabolic outcomes, including insulin resistance, adipose tissue distribution, adipocyte morphometry, and expression of inflammatory markers in adipose tissue as well as to assess whether postnatal overfeeding would exacerbate these effects. Findings indicate that prenatal BPA exposure leads to insulin resistance in adulthood in the first breeder cohort ( study 1), but not in the second cohort ( study 2), which is suggestive of potential differences in genetic susceptibility. BPA exposure induced adipocyte hypertrophy in the visceral fat depot without an accompanying increase in visceral fat mass or increased CD68, a marker of macrophage infiltration, in the subcutaneous fat depot. Cohens effect size analysis found the ratio of visceral to subcutanous fat depot in the prenatal BPA-treated overfed group to be higher compared with the control-overfed group. Altogether, these results suggest that exposure to BPA during fetal life at levels found in humans can program metabolic outcomes that lead to insulin resistance, a forerunner of type 2 diabetes, with postnatal obesity failing to manifest any interaction with prenatal BPA relative to insulin resistance and adipocyte hypertrophy.

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Effect of date of mating and housing on lamb growth, adipose tissue deposition and plasma leptin concentrations

Proceedings of the British Society of Animal Science ◽

10.1017/s1752756200007420 ◽

2002 ◽

Vol 2002 ◽

pp. 86-86

Author(s):

S. Pearce ◽

A. Mostyn ◽

E. Genever ◽

D.H. Keisler ◽

R. Webb ◽

...

Keyword(s):

Adipose Tissue ◽

Birth Weight ◽

Brown Adipose Tissue ◽

Uncoupling Protein ◽

Physiological Role ◽

Fetal Life ◽

Brown Adipose ◽

Adipose Tissue Development ◽

Plasma Leptin ◽

Sheep Fetus

In lambs, the rapid increase in heat production after birth is due to initiation of nonshivering thermogenesis in brown adipose tissue (BAT). This occurs in conjunction with an increase in amount and activity of BAT specific uncoupling protein 1 (UCP1) (Clarke et al. 1997). UCP1 abundance and activity is low in fetal life but, within twelve hours of birth, there is an increase in the thermogenic activity of BAT and mRNA for UCP1. This ontogeny of UCP1 mRNA in BAT is very similar that of leptin, which is first detectable in the sheep fetus at 90 days gestation in fetal adipose tissue, its expression then increases up to term at 147 days (Yuen et al 1999). Leptin is a hormone which is thought to play a physiological role is in energy balance, it is primarily produced by white adipose tissue although there is evidence for its production in both brown adipose tissue and the placenta. Lambs born in the autumn are known to be smaller than those born in the spring (McCoard et al. 1997). It is not known if moderate changes in date of mating can influence birth weight or adipose tissue development. The present study aimed to determine whether date of mating could influence lamb birth weight, the abundance of BAT, UCP1, plasma leptin.

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Development and regulation of glucose transporter and hexokinase expression in rat

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1994.266.4.e548 ◽

1994 ◽

Vol 266 (4) ◽

pp. E548-E559 ◽

Cited By ~ 17

Author(s):

C. Postic ◽

A. Leturque ◽

R. L. Printz ◽

P. Maulard ◽

M. Loizeau ◽

...

Keyword(s):

Adipose Tissue ◽

Insulin Sensitivity ◽

Brown Adipose Tissue ◽

Glucose Transporter ◽

Fetal Liver ◽

Rat Tissues ◽

Fetal Life ◽

Glut 1 ◽

Glut 4 ◽

Brown Adipose

The ontogenesis of the glucose transporters GLUT-1, GLUT-2, and GLUT-4 and the hexokinases HK-I, HK-II, and HK-IV (glucokinase) was studied in rat tissues. In brown adipose tissue, high levels of GLUT-4 and HK-II were observed during fetal life; both decreased at birth and then increased throughout development. At birth, cold exposure increased GLUT-4 and HK-II expression in brown adipose tissue, whereas fasting decreased it. GLUT-1 and HK-I were present in fetal muscle, but GLUT-4 and HK-II were absent. The coordinate appearance of GLUT-4 and HK-II in skeletal muscle was concomitant with the acquisition of insulin sensitivity after weaning. In the heart, the glucose transporter isoform switched from GLUT-1 to GLUT-4 during the suckling period. The coordinate expression of GLUT-4 and HK-II in heart was observed after weaning. GLUT-2, detected in fetal liver, increased throughout development. GLUT-1 and HK-I were detectable in fetal liver, whereas glucokinase appeared after weaning. Consumption of a high-carbohydrate diet after weaning increased GLUT-4 and HK-II in muscle and GLUT-2 in liver, whereas consumption of a high-fat diet prevented these changes. These results showed that 1) GLUT-1 and HK-I are abundant in most fetal rat tissues, 2) GLUT-4 and HK-II expression is associated with the appearance of tissue insulin sensitivity, and 3) GLUT-2 is expressed early in liver, before the appearance of glucokinase.

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