Abundance of leptin mRNA in fetal adipose tissue is related to fetal body weight

Yuen, B. S. J.; McMillen, I. C.; Symonds, Michael; Owens, Philip

doi:10.1677/joe.0.163r011

Cited by 73 publications

(61 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The increase in the abundance of LEP mRNA in intermuscular AT may reflect an enhanced ability to synthesize LEP, which could in turn sustain the increase in plasma LEP levels from 210 dpc onwards, at least in Charolais foetuses. In line with our results, an increase in LEP mRNA abundances in perirenal AT (Yuen et al, 1999) and plasma LEP (Yuen et al, 2003) was reported in ovine foetuses during the last month before birth.…”

Section: Discussionsupporting

confidence: 93%

Foetal bovine intermuscular adipose tissue exhibits histological and metabolic features of brown and white adipocytes during the last third of pregnancy

Taga

Chilliard

Picard

et al. 2012

Animal

View full text Add to dashboard Cite

This study reports the metabolic and morphological characteristics of bovine intermuscular adipose tissue (AT) throughout foetal growth. Our hypothesis was that the histological and molecular features of intermuscular AT would be different from those previously reported for foetal perirenal AT, based on its anatomical location near the muscle and the recent identification of two distinct adipocyte precursors in mouse AT depending on their locations. To address this question, intermuscular AT was sampled from Charolais and Blond d'Aquitaine foetuses at 180, 210 and 260 days post conception (dpc). The two bovine breeds were chosen because of the higher adiposity of Charolais than Blond d'Aquitaine cattle during the postnatal life. Regardless of the breed, adipocyte volume increased slightly (138%, P , 0.01) with increasing foetal age. This was concomitant with a decrease ( P , 0.05) in the activity of enzymes involved in de novo fatty acid (FA) synthesis (FA synthase and glucose-6-phosphate dehydrogenase) and FA esterification (glycerol-3-phosphate dehydrogenase) when expressed per million adipocytes, and with an increase ( P < 0.01) in mRNA abundances for uncoupling protein 1, adiponectin and leptin (LEP) between 180 and 260 dpc. No difference was observed in the adipocyte volume between breeds, which was consistent with the lack of major between-breed differences in mRNA abundances or activities of enzymes involved in lipid metabolism. The mRNA abundance of lipoprotein lipase was maintained across ages, suggesting a storage of circulating FA rather than of FA synthesized de novo. Plasma LEP increased with foetal age, but only in the Charolais breed (171%, P < 0.01), and was two-to threefold higher in Charolais than Blond d'Aquitaine foetuses. Regardless of the breed, bovine intermuscular AT contained predominantly unilocular adipocytes believed to be white adipocytes that were larger at 260 dpc than at 180 dpc. These data thus challenge current concepts of the largely brown nature of bovine foetal AT (based on histological and metabolic features of perirenal AT as previously reported a few days before or after birth).

show abstract

Section: Discussionsupporting

confidence: 93%

Foetal bovine intermuscular adipose tissue exhibits histological and metabolic features of brown and white adipocytes during the last third of pregnancy

Taga

Chilliard

Picard

et al. 2012

Animal

View full text Add to dashboard Cite

show abstract

“…The negative relationships between birthweight and subsequent leptin production in adulthood are the opposite of the reported positive correlations seen between body weight and leptin production in fetuses (21) and infants (11±14). Maternal nutrition during pregnancy in¯uences the body weight of the fetus (22±24) and, in female pigs, plasma leptin concentrations are higher in progeny from mothers provided with more feed (25).…”

Section: Introductionmentioning

confidence: 65%

Maternal glucocorticoid treatment modulates placental leptin and leptin receptor expression and materno-fetal leptin physiology during late pregnancy, and elicits hypertension associated with hyperleptinaemia in the early-growth-retarded adult offspring

Sugden

Langdown²,

Munns³

et al. 2001

European Journal of Endocrinology

120

View full text Add to dashboard Cite

Background: Leptin concentrations are increased during late pregnancy, and leptin receptors are expressed in placental and fetal tissues, suggesting a role for leptin in placental and/or fetal growth, or both. In humans, leptin concentrations in adulthood are inversely related to body weight at birth, independent of adult adiposity, and correlate with fasting insulin. Glucocorticoids and insulin regulate leptin secretion. Excessive exposure to glucocorticoids during late fetal development in the rat causes intrauterine growth retardation (IUGR), together with hypertension and hyperinsulinaemia in adulthood. Leptin may have a role in the development of some forms of hypertension. Objective: To determine whether IUGR induced by maternal glucocorticoid treatment during the last third of pregnancy in the rat is associated with modulation of either maternal or fetal leptin concentrations, the placental expression of leptin or the short form of the leptin receptor (ObR-S), or combinations thereof, and to evaluate whether hypertension or hyperinsulinaemia in the earlygrowth-retarded adult progeny of dexamethasone-treated dams is associated with altered leptin concentrations. Design and Methods: Dexamethasone was administered to pregnant rats from day 15 to day 21 of gestation via a chronically implanted subcutaneous osmotic minipump. Protein expression of leptin and ObR-S in the placenta at day 21 of pregnancy was measured by western blotting. Plasma leptin and insulin concentrations were determined by radioimmunoassay and ELISA respectively. Systolic hypertension was measured by tail cuff plethysmography. Results: Dexamethasone administration during the last third of pregnancy decreased placental mass and fetal body weight at day 21 of gestation, caused maternal hyperleptinaemia but fetal hypoleptinaemia, and suppressed placental leptin protein expression whilst up-regulating placental protein expression of ObR-S. The male and female offspring of dexamethasone-treated dams were hypertensive from 12 weeks of age. One-year-old offspring of dexamethasone-treated dams exhibited signi®cant hyperleptinaemia compared with age-matched controls, an effect associated with hyperinsulinaemia in the male, but not female, offspring. Conclusions: The rat model of maternal dexamethasone treatment is established as a paradigm of programmed' hypertension in man. Our data show modi®cation of placental leptin and leptin receptor protein expression by dexamethasone treatment during the last third of pregnancy. We also show that leptin concentrations are suppressed during fetal life but increased in adulthood in this rat model of programmed hypertension. Our data do not necessarily establish a causal relationship between fetal hypoleptinaemia and impaired fetal growth during early life, or between hyperleptinaemia and hypertension in adulthood. Nevertheless, they suggest that hyperleptinaemia may be a component of the cluster of metabolic abnormalities seen in the insulin resistance syndrome in man. They also suggest that excessive...

show abstract

“…In one study, fetal plasma leptin was positively correlated with plasma cortisol, but inversely correlated with PaO2 [31]. Fetal body weight was shown to be inversely related to plasma leptin concentrations in one study [32] but in another [33] body weight was positively correlated with leptin mRNA, which strongly correlates with plasma leptin [34]. We have not [12] and in 70-75 year old men and women [10].…”

Section: Body Compositionmentioning

confidence: 73%

Long Term Consequences of Low Birthweight on Postnatal Growth, Adiposity and Brain Weight at Maturity in Sheep

Louey

Cock

Harding

2005

Journal of Reproduction and Development

View full text Add to dashboard Cite

Abstract. Low birth weight (LBW) as a result of restricted fetal growth increases the risk for later metabolic diseases and adiposity. However the relationship between LBW and postnatal growth and adult body composition has not been fully investigated. We have used sheep to determine the effects of LBW on postnatal growth and body composition at maturity. LBW was induced by twinning and placental embolization. At birth, LBW lambs were 38% lighter than controls (2.8 ± 0.2 vs 4.4 ± 0.3 kg, P<0.05), but had caught up in bodyweight by 8 weeks after birth. At ~2.3 years, bodyweights were not different between groups, but there were reductions in absolute (-8%) and relative (-17%) brain weights of LBW sheep (P<0.05) compared to controls. X-ray absorptiometry showed that the mature LBW sheep, compared to controls, had greater amounts of lean muscle (38.1 ± 1.3 vs 35.3 ± 0.5 kg, P<0.05) and tended to have more body fat (12.2 ± 1.2 vs 9.6 ± 0.9 kg; P=0.1); at autopsy abdominal fat mass was greater in LBW sheep (3.06 ± 0.26 vs 2.20 ± 0.25 kg, P<0.05). Plasma leptin concentrations were not different between groups. We conclude that, in sheep, LBW is associated with early postnatal catch-up in body weight, but body composition is permanently altered such that, relative to controls, adiposity is increased and brain weight is decreased. Key words: Adiposity, Fetal growth restriction, Body composition, Birth weight, Leptin (J. Reprod. Dev. 51: [59][60][61][62][63][64][65][66][67][68] 2005) he postnatal effects of low birth weight (LBW) are of considerable interest because in recent years LBW has been associated with an increased risk of several adult-onset diseases [1][2][3]. LBW, especially that caused by restricted fetal growth, is often followed by accelerated postnatal growth [4], and recent studies indicate that this catch-up growth can amplify the risk for cardiovascular and metabolic dysfunction. Individuals who had low birth weights but exhibited increased growth rates in terms of weight, height or body mass index (BMI) have been shown to be at a greater risk for abdominal adiposity [5], hypertension [2, 3] and non-insulin dependent diabetes mellitus [6] than those who failed to catch up [7].As well as differing postnatal growth rates, body c o m p o si t i o n c a n d i f f e r b e t w e e n L B W a n d appropriately grown individuals. At birth, LBW infants have reduced body fat, lean mass and bone m i n e r a l c o n t e n t ( B M C ) c o m p a r e d w i t h appropriately grown newborns [8]. However, these reductions are related to lower body weights, and body composition is not different between LBW and normally grown infants of similar weights [8]. After birth, age-related changes in body composition differ between LBW and appropriately grown infants. For example, the postnatal increase in BMC in LBW infants is less than that of appropriately grown infants [9], and adults of low birth weight have reduced total BMC and reduced bone mineral density (BMD) [10]. Adiposity is also affected, such that body fat content...

show abstract

Abundance of leptin mRNA in fetal adipose tissue is related to fetal body weight

Cited by 73 publications

References 29 publications

Foetal bovine intermuscular adipose tissue exhibits histological and metabolic features of brown and white adipocytes during the last third of pregnancy

Foetal bovine intermuscular adipose tissue exhibits histological and metabolic features of brown and white adipocytes during the last third of pregnancy

Maternal glucocorticoid treatment modulates placental leptin and leptin receptor expression and materno-fetal leptin physiology during late pregnancy, and elicits hypertension associated with hyperleptinaemia in the early-growth-retarded adult offspring

Long Term Consequences of Low Birthweight on Postnatal Growth, Adiposity and Brain Weight at Maturity in Sheep

Contact Info

Product

Resources

About