Brown adipose tissue in the parametrial fat pad of the mouse

Young, P.; Arch, Jonathan R.S.; Ashwell, Margaret

doi:10.1016/0014-5793(84)80822-4

Cited by 343 publications

(247 citation statements)

References 15 publications

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“…Previous studies found brown fat emergence in WAT coupled with enhanced whole-body energy expenditure, but these studies used non-dietary manipulations, including chronic exposure to cold, treatment with b3-adrenergic receptor agonists and forced WAT overexpression of key molecules of brown fat adipogenesis/function, such as PGC-1a, UCP1 or PRDM16. 12,14,18,20,[39][40][41][42] Brown fat adipogenesis has recently gained the interest of many research groups, as compelling evidence has been provided that brown fat exists not only in human neonates, as thought originally, but also in human adults where it likely protects against obesity, 2-8 through its superior capacity for burning fat (both stored and eaten) and energy dissipation. 9,43 Substantial progress in our understanding of brown fat adipogenesis has been made recently (Seale et al 43 ).…”

Section: Discussionmentioning

confidence: 99%

High-fat diet induces emergence of brown-like adipocytes in white adipose tissue of spontaneously hypertensive rats

et al. 2011

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Obesity has a profound adverse impact on health. In this study, we present evidence for high-fat diet (HFD)-induced emergence of brown-like adipocytes in white adipose tissue (WAT) of the spontaneously hypertensive rat (SHR). We studied adult males fed a HFD or normal diet (ND) for 12 weeks. At the end of the 12-week dietary intervention, HFD compared with ND rats showed significantly higher whole-body energy expenditure. HFD vs. ND rats also showed higher expression of genes involved in fatty acid oxidation, mitochondrial biogenesis and brown fat adipogenesis, as well as augmented mitochondrial mass in WAT but not in the liver or skeletal muscle. Consistent with the molecular changes, in HFD but not in ND rats, histological and immunohistochemistry-based analyses of WAT demonstrated the presence of small multilocular cells staining positively for uncoupling protein 1, indicating the emergence of brown-like adipocytes in WAT. Our results suggest that SHR may have the capacity to increase energy expenditure in response to a chronic HFD that may be linked to the emergence of brown-like adipocytes in WAT. Thus, the SHR may be an important genetic model to uncover novel mechanisms of resistance to dietary obesity.

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Section: Discussionmentioning

confidence: 99%

High-fat diet induces emergence of brown-like adipocytes in white adipose tissue of spontaneously hypertensive rats

et al. 2011

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“…11 The first use of the term 'beige', to our knowledge, was by the Seale laboratory 12 in a commentary about a paper by Vegiopoulos et al 13 The first reports of the presence of 'brown adipocytes' among white adipocytes in traditionally white adipocyte depots to our knowledge, however, occurred 26 years earlier in the pioneering studies of Young et al 14 They reported brown adipocytes in the parametrial WAT pad of BALB/c mice acclimated to the cold, as identified morphologically by light and electron microscopy, and as possessing increases in a marker of brown adipocytes, mitochondrial UCP-1 content, 14 the finding of which the field and we turned a blind eye toward because such a presence was almost heretical, given the Zeitgeist of the time that WAT and BAT were separate tissues with separate functions. Loncar et al 15 soon after reported that young (10-13 weeks old) domestic cats exposed to − 30°C for 1 h twice a day during a week displayed brown-like adipocyte changes, most notably increases in mitochondria volume and surface density of mitochondrial cristae in several WAT depots not seen in the room temperature controls and more typical of brown adipocytes, not white ones.…”

Section: Methodsmentioning

confidence: 99%

Neural control of white, beige and brown adipocytes

Bartness

Ryu

2015

Int J Obes Supp

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Reports of brown-like adipocytes in traditionally white adipose tissue (WAT) depots occurred~30 years ago, but interest in white adipocyte 'browning' only has gained attention more recently. We integrate some of what is known about the sympathetic nervous system (SNS) innervation of WAT and brown adipose tissue (BAT) with the few studies focusing on the sympathetic innervation of the so-called 'brite' or 'beige' adipocytes that appear when WAT sympathetic drive increases (for example, cold exposure and food deprivation). Only one brain site, the dorsomedial hypothalamic nucleus (DMH), selectively browns some (inguinal WAT (IWAT) and dorsomedial subcutaneous WAT), but not all WAT depots and only when DMH neuropeptide Y gene expression is knocked down, a browning effect is mediated by WAT SNS innervation. Other studies show that WAT sympathetic fiber density is correlated with the number of brown-like adipocytes (multilocular lipid droplets, uncoupling protein-1 immunoreactivity) at both warm and cold ambient temperatures. WAT and BAT have sensory innervation, the latter important for acute BAT cold-induced temperature increases, therefore suggesting the possible importance of sensory neural feedback from brite/beige cells for heat production. Only one report shows browned WAT capable of producing heat in vivo. Collectively, increases in WAT sympathetic drive and the phenotype of these stimulated adipocytes seems critical for the production of new and/or transdifferentiation of white to brite/ beige adipocytes. Selective harnessing of WAT SNS drive to produce browning or selective browning independent of the SNS to counter increases in adiposity by increasing expenditure appears to be extremely challenging.

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“…UCP1 is usually only expressed in significant amounts in BAT and not in WAT, so that the appearance of this protein in WAT is considered as a sign of a transdifferentiation process, that is, the conversion of WAT in a tissue with cellular similarities to BAT. Acquirement of BAT-like features by WAT can be provoked by physiological conditions, such as cold stress, 22 or by pharmacological intervention, such as b 3 -adrenergic stimulation. 23 Moreover, UCP1 expression in WAT is related to body weight loss in obese and UCP1 transgenic mice 24,25 and can also occur in human white adipocytes.…”

Section: Effect Of C18 Fatty Acids On Body Weight O Vögler Et Almentioning

confidence: 99%

Structure–effect relation of C18 long-chain fatty acids in the reduction of body weight in rats

et al. 2007

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Objective: To investigate the relationship between chemical structure and physiological effect, the efficacy and the molecular mechanisms involved in the reduction of body weight by C18 fatty acids (stearic, elaidic, oleic, linoleic and 2-hydroxyoleic acids (2-OHOA)). Design: Ad libitum fed, lean Wistar Kyoto rats treated orally with up to 600 mg kg À1 of the fatty acids or vehicle every 12 h for 7 days. Besides, starved rats and rats pairfed to the 2-OHOA-treated group served as additional controls under restricted feeding conditions. Measurements: Body weight, food intake, weight of various fat depots, plasma leptin, hypothalamic neuropeptides, uncoupling proteins (UCP) in white (WAT) and brown adipose tissue (BAT) and phosphorylation level of cyclic AMP (cAMP) response element-binding protein (CREB) in WAT. Results: Only treatment with oleic acid and 2-OHOA induced body weight loss (3.3 and 11.4%, respectively) through reduction of adipose fat mass. Food intake in these rats was lower, although hypothalamic neuropeptide and plasma leptin levels indicated a rise in orexigenic status. Rats pairfed to the 2-hydroxyoleic group only lost 6.3% body weight. UCP1 expression and phosphorylation of CREB was drastically increased in WAT, but not BAT of 2-OHOA-treated rats, whereas no UCP1 expression could be detected in WAT of rats treated with oleic acid. Conclusion: Both cis-configured monounsaturated C18 fatty acids (oleic acid and 2-OHOA) reduce body weight, but the introduction of a hydroxyl group in position 2 drastically increases loss of adipose tissue mass. The novel molecular mechanism unique to 2-hydroxyoleic, but not oleic acid, implies induction of UCP1 expression in WAT by the cAMP/PKA pathwaydependent transcription factor CREB, most probably as part of a transdifferentiation process accompanied by enhanced energy expenditure.

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Brown adipose tissue in the parametrial fat pad of the mouse

Cited by 343 publications

References 15 publications

High-fat diet induces emergence of brown-like adipocytes in white adipose tissue of spontaneously hypertensive rats

High-fat diet induces emergence of brown-like adipocytes in white adipose tissue of spontaneously hypertensive rats

Neural control of white, beige and brown adipocytes

Structure–effect relation of C18 long-chain fatty acids in the reduction of body weight in rats

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