The early development of white adipose tissue. Effects of litter size on the lipoprotein lipase activity of four adipose-tissue depots, serum immunoreactive insulin and tissue cellularity during the first four weeks of life in the rat

Cryer, Anthony; Jones, Heather M.

doi:10.1042/bj1780711

Cited by 29 publications

(28 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Excess adiposity gain in RE rats after HF diet was attributable to excess adipocyte hyperplasia, rather than excess adipocyte hypertrophy and, interestingly, an increased cell proliferation potential was found in WAT of young RE rats at weaning. Importantly, total retinol levels in WAT of WAT development in the rat takes place within the first 30 days of postnatal life, 47 and excess vitamin A within this period elicited changes in the developing tissue. In particular, iWAT of RE-treated rats at weaning was enriched in small adipocytes and in PCNA, a classical marker of proliferative status, while displaying a reduced expression of the master adipogenic transcription factor PPARg and its downstream target, lipoprotein lipase .…”

Section: Discussionmentioning

confidence: 99%

Vitamin A supplementation in early life affects later response to an obesogenic diet in rats

et al. 2012

View full text Add to dashboard Cite

OBJECTIVE:To assess the influence of supplementation with a moderate dose of vitamin A in early life on adipose tissue development and the response to an obesogenic diet later in life. METHODS: During the suckling period, rat pups received a daily oral dose of retinyl palmitate corresponding to three times the vitamin A ingested daily from maternal milk. Control rats received the vehicle (olive oil). Short-term effects of treatment on gene expression and morphology of white adipose tissue (WAT) were analyzed in animals on the day after weaning (day 21). To study long-term effects, control and vitamin A-treated rats were fed, after weaning, a normal fat or a high-fat (HF) diet for 16 weeks. RESULTS: WAT of vitamin A-treated young rats (day 21) was enriched in small adipocytes with a reduced expression of adipogenic markers (peroxisome proliferator-activated receptor g and lipoprotein lipase) and an increased cell proliferation potential as indicated by increased expression of proliferating cell nuclear antigen. Increased retinoic acid (RA)-induced transcriptional responses were present in the tissues of vitamin A-treated young rats (day 21) including WAT. Vitamin A-treated rats developed higher adiposity than control rats on a HF diet as indicated by body composition analysis and increased WAT depot mass, adipocyte diameter, WAT DNA content, leptinemia and adipose leptin gene expression. Excess adiposity gain in vitamin A-treated rats developed in the absence of changes in body weight and was attributable to excess adipocyte hyperplasia. No differences in adiposity were observed between vitamin A-treated rats and control rats on a normal fat diet. Total retinol levels in WAT of vitamin A-treated rats were elevated at weaning (day 21) and normalized by day 135 of age. CONCLUSION: Vitamin A intake in the early stages of postnatal life favors subsequent HF diet-induced adiposity gain through mechanisms that may relate to changes in adipose tissue development, likely mediated by RA.

show abstract

Section: Discussionmentioning

confidence: 99%

Vitamin A supplementation in early life affects later response to an obesogenic diet in rats

et al. 2012

View full text Add to dashboard Cite

show abstract

“…In this model, rats raised in small litters (3-4 pups per mother) ingest larger amounts of milk (11) and gain more body weight than rats raised in normal or large litters (8 or more rats/mother). Interestingly, the increased body weight of the rats growing in small litters continues even after weaning (9,10,(12)(13)(14)(15)(16)(17). Hypothalamic and neuroendocrine axis changes and a permanent reprogramming of thermogenesis in the brown adipose tissue may contribute to a persistent increase of the visceral fat deposits and to body weight gain in animals submitted to overfeeding in the early phases of postnatal life (9,10,18,19).…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic treadmill training on body mass gain and visceral fat accumulation in overfed rats

Dantas

Pimentel

Gonçalves

et al. 2010

Braz J Med Biol Res

View full text Add to dashboard Cite

This study evaluated the effects of chronic treadmill training on body mass gain and visceral fat accumulation in overfed rats. Overfeeding was induced by reducing the litter size to 3 male pups per mother during the suckling period. The litter size of control rats was adjusted to 10 male pups per mother. Seven weeks after birth overfed and normally fed rats were selected and assigned to a sedentary protocol or to a low-intensity treadmill training protocol (60 min, 5 times/week, for 9 weeks). Four groups (overfed sedentary, N = 23; normally fed sedentary, N = 32; overfed exercised, N = 18, and normally fed exercised, N = 18) were evaluated at 18 weeks. Data are reported as means ± SEM. Initial body weight was similar in control and overfed rats [8.0 ± 0.2 g (N = 42) vs 8.0 ± 0.1 g (N = 50); P > 0.05] and body weight gain during the suckling period was higher in the overfed rats (30.6 ± 0.9 vs 23.1 ± 0.3 g; P < 0.05). Exercise attenuated the body weight gain of overfed compared to sedentary rats (505 ± 14 vs 537 ± 12 g; P < 0.05). The sedentary overfed rats showed higher visceral fat weight compared to normally fed animals (31.22 ± 2.08 vs 21.94 ± 1.76 g; P < 0.05). Exercise reduced visceral fat by 36.5% in normally fed rats and by 35.7% in overfed rats. Exercise attenuated obesity in overfed rats and induced an important reduction of visceral fat.

show abstract

“…Suckling period overnutrition permanently alters body-weight regulation and glucose metabolism of SL rodents. Although all pups are provided the same diet (ad lib) after weaning, SL offspring remain heavier and fatter in adulthood (25,26) , and exhibit impaired glucose tolerance (24,27) and dysregulated endocrine pancreas function (27) . We performed metabolic cage studies to determine if the persistent change in energy balance regulation of SL mice is caused by altered food intake or energy expenditure (28) .…”

mentioning

confidence: 99%

Developmental programming of energy balance regulation: is physical activity more ‘programmable’ than food intake?

et al. 2015

View full text Add to dashboard Cite

Extensive human and animal model data show that environmental influences during critical periods of prenatal and early postnatal development can cause persistent alterations in energy balance regulation. Although a potentially important factor in the worldwide obesity epidemic, the fundamental mechanisms underlying such developmental programming of energy balance are poorly understood, limiting our ability to intervene. Most studies of developmental programming of energy balance have focused on persistent alterations in the regulation of energy intake; energy expenditure has been relatively underemphasised. In particular, very few studies have evaluated developmental programming of physical activity. The aim of this review is to summarise recent evidence that early environment may have a profound impact on establishment of individual propensity for physical activity. Recently, we characterised two different mouse models of developmental programming of obesity; one models fetal growth restriction followed by catchup growth, and the other models early postnatal overnutrition. In both studies, we observed alterations in body-weight regulation that persisted to adulthood, but no group differences in food intake. Rather, in both cases, programming of energy balance appeared to be due to persistent alterations in energy expenditure and spontaneous physical activity (SPA). These effects were stronger in female offspring. We are currently exploring the hypothesis that developmental programming of SPA occurs via induced sexspecific alterations in epigenetic regulation in the hypothalamus and other regions of the central nervous system. We will summarise the current progress towards testing this hypothesis. Early environmental influences on establishment of physical activity are likely an important factor in developmental programming of energy balance. Understanding the fundamental underlying mechanisms in appropriate animal models will help determine whether early life interventions may be a practical approach to promote physical activity in man.Metabolic imprinting: Epigenetics: DNA methylation: Nutrition Developmental programming, epigenetics and obesity During critical periods of embryonic, fetal and early postnatal development, environmental influences can affect mammalian development, leading to permanent changes in the regulation of energy balance. There is increasing acceptance of the idea that such developmental programming of energy balance regulation is an †These authors contributed equally to this work.

show abstract

The early development of white adipose tissue. Effects of litter size on the lipoprotein lipase activity of four adipose-tissue depots, serum immunoreactive insulin and tissue cellularity during the first four weeks of life in the rat

Cited by 29 publications

References 55 publications

Vitamin A supplementation in early life affects later response to an obesogenic diet in rats

Vitamin A supplementation in early life affects later response to an obesogenic diet in rats

Effects of chronic treadmill training on body mass gain and visceral fat accumulation in overfed rats

Developmental programming of energy balance regulation: is physical activity more ‘programmable’ than food intake?

Contact Info

Product

Resources

About