scholarly journals The adipose organ: morphological perspectives of adipose tissues

2001 ◽  
Vol 60 (3) ◽  
pp. 319-328 ◽  
Author(s):  
Saverio Cinti
Keyword(s):  
Adipose Tissue ◽  
Uncoupling Protein ◽  
Gross Anatomy ◽  
Cell Types ◽  
Vascular Supply ◽  
Adipose Tissues ◽  
White Adipocyte ◽  
Metabolic Functions ◽  
Brown Adipose ◽  
Adipose Organ

Anatomically, an organ is defined as a series of tissues which jointly perform one or more interconnected functions. The adipose organ qualifies for this definition as it is made up of two tissue types, the white and brown adipose tissues, which collaborate in partitioning the energy contained in lipids between thermogenesis and the other metabolic functions. In rats and mice the adipose organ consists of several subcutaneous and visceral depots. Some areas of these depots are brown and correspond to brown adipose tissue, while many are white and correspond to white adipose tissue. The number of brown adipocytes found in white areas varies with age, strain of animal and environmental conditions. Brown and white adipocyte precursors are morphologically dissimilar. Together with a rich vascular supply, brown areas receive abundant noradrenergic parenchymal innervation. The gross anatomy and histology of the organ vary considerably in different physiological (cold acclimation, warm acclimation, fasting) and pathological conditions such as obesity; many important genes, such as leptin and uncoupling protein-1, are also expressed very differently in the two cell types. These basic mechanisms should be taken into account when addressing the physiopathology of obesity and its treatment.

scholarly journals Endothelial cell crosstalk improves browning but hinders white adipocyte maturation in 3D engineered adipose tissue

2020 ◽  
Vol 12 (4) ◽  
pp. 81-89
Author(s):  
Jennifer H Hammel ◽  
Evangelia Bellas
Keyword(s):  
Endothelial Cells ◽  
Adipose Tissue ◽  
Type I Collagen ◽  
Network Formation ◽  
Uncoupling Protein ◽  
Collagen Gel ◽  
Cell Types ◽  
Vascular Network ◽  
Type I ◽  
White Adipocyte

Abstract Central to the development of adipose tissue (AT) engineered models is the supporting vasculature. It is a key part of AT function and long-term maintenance, but the crosstalk between adipocytes and endothelial cells is not well understood. Here, we directly co-culture the two cell types at varying ratios in a 3D Type I collagen gel. Constructs were evaluated for adipocyte maturation and function and vascular network organization. Further, these constructs were treated with forskolin, a beta-adrenergic agonist, to stimulate lipolysis and browning. Adipocytes in co-cultures were found to be less mature than an adipocyte-only control, shown by smaller lipid droplets and downregulation of key adipocyte-related genes. The most extensive vascular network formation was found in the 1:1 co-culture, supported by vascular endothelial growth factor (VEGF) upregulation. After forskolin treatment, the presence of endothelial cells was shown to upregulate PPAR coactivator 1 alpha (PGC-1α) and leptin, but not uncoupling protein 1 (UCP1), suggesting a specific crosstalk that enhances early stages of browning.

Thermogenic effect of triiodothyroacetic acid at low doses in rat adipose tissue without adverse side effects in the thyroid axis

2008 ◽  
Vol 294 (4) ◽  
pp. E688-E697 ◽  
Author(s):  
G. Medina-Gomez ◽  
R. M. Calvo ◽  
M.-J. Obregon
Keyword(s):  
Adipose Tissue ◽  
Cold Exposure ◽  
Uncoupling Protein ◽  
Thyroid Stimulating Hormone ◽  
Low Doses ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Thyroid Axis ◽  
Rat Adipose Tissue

Triiodothyroacetic acid (TRIAC) is a physiological product of triiodothyronine (T3) metabolism, with high affinity for T3 nuclear receptors. Its interest stems from its potential thermogenic effects. Thus this work aimed 1) to clarify these thermogenic effects mediated by TRIAC vs. T3 in vivo and 2) to determine whether they occurred predominantly in adipose tissues. To examine this, control rats were infused with equimolar T3 or TRIAC doses (0.8 or 4 nmol·100 g body wt−1·day−1) or exposed for 48 h to cold. Both T3 doses and only the highest TRIAC dose inhibited plasma and pituitary thyroid-stimulating hormone (TSH) and thyroxine (T4) in plasma and tissues. Interestingly, the lower TRIAC dose marginally inhibited plasma T4. T3 infusion increased plasma and tissue T3 in a tissue-specific manner. The highest TRIAC dose increased TRIAC concentrations in plasma and tissues, decreasing plasma T3. TRIAC concentrations in tissues were <10% those of T3. Under cold exposure or high T3 doses, TRIAC increased only in white adipose tissue (WAT). Remarkably, only the lower TRIAC dose activated thermogenesis, inducing ectopic uncoupling protein (UCP)-1 expression in WAT and maximal increases in UCP-1, UCP-2, and lipoprotein lipase (LPL) expression in brown adipose tissue (BAT), inhibiting UCP-2 in muscle and LPL in WAT. TRIAC, T3, and cold exposure inhibited leptin secretion and mRNA in WAT. In summary, TRIAC, at low doses, induces thermogenic effects in adipose tissues without concomitant inhibition of TSH or hypothyroxinemia, suggesting a specific role regulating energy balance. This selective effect of TRIAC in adipose tissues might be considered a potential tool to increase energy metabolism.

Nicotine infusion alters leptin and uncoupling protein 1 mRNA expression in adipose tissues of rats

2001 ◽  
Vol 280 (6) ◽  
pp. E867-E876 ◽  
Author(s):  
Keiko Arai ◽  
Kyongsong Kim ◽  
Katsumi Kaneko ◽  
Mitsue Iketani ◽  
Asuka Otagiri ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mrna Expression ◽  
Wistar Rats ◽  
Uncoupling Protein ◽  
Plasma Concentrations ◽  
Uncoupling Protein 1 ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Male Wistar Rats ◽  
Infusion Period

We attempted to clarify whether leptin and uncoupling protein 1 (UCP1) are involved in the action of nicotine on the energy balance. Male Wistar rats were infused subcutaneously with nicotine (12 mg · kg−1 · day−1) for 4 or 14 days. At the end of the 4-day period, the plasma concentrations of leptin of the nicotine-treated and pair-fed rats were lower than those of the freely fed rats, although the levels of leptin mRNA expression in various white adipose tissues did not differ among the three groups. At the end of the 14-day nicotine infusion period, plasma concentrations of leptin were higher, and leptin mRNA expression in the omentum and epididymal and retroperitoneal adipose tissues was stronger in the nicotine-treated rats than in the pair-fed and freely fed rats. UCP1 mRNA expression in the brown adipose tissue of nicotine-treated was stronger than that of the pair-fed rats. These results suggest that continuous nicotine infusion differentially affects the synthesis and secretion of leptin according to the duration of infusion and stimulates UCP1 mRNA expression, probably in a manner independent of leptin.

Thyroid-stimulating hormone receptor in brown adipose tissue is involved in the regulation of thermogenesis

2008 ◽  
Vol 295 (2) ◽  
pp. E514-E518 ◽  
Author(s):  
Toyoshi Endo ◽  
Tetsuro Kobayashi
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Brown Adipose Tissue ◽  
Rectal Temperature ◽  
Hormone Receptor ◽  
Uncoupling Protein ◽  
Thyroid Stimulating Hormone ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
Stimulating Hormone

C.RF- Tshrhyt/hyt mice have a mutated thyroid-stimulating hormone receptor (TSHR), and, without thyroid hormone supplementation, these mice develop severe hypothyroidism. When hypothyroid Tshrhyt/hyt mice were exposed to cold (4°C), rectal temperature rapidly dropped to 23.9 ± 0.40°C at 90 min, whereas the wild-type mice temperatures were 37.0 ± 0.15°C. When we carried out functional rat TSHR gene transfer in the brown adipose tissues by plasmid injection combined with electroporation, there was no effect on the serum levels of thyroxine, although rectal temperature of the mice transfected with pcDNA3.1/Zeo-rat TSHR 90 min after cold exposure remained at 34.6 ± 0.34°C, which was significantly higher than that of Tshrhyt/hyt mice. Transfection of TSHR cDNA increased mRNA and protein levels of uncoupling protein-1 (UCP-1) in brown adipose tissues, and the weight ratio of brown adipose tissue to overall body weight also increased. Exogenous thyroid hormone supplementation to Tshrhyt/hyt mice restored rectal temperature 90 min after exposure to cold (36.8 ± 0.10°C). These results indicate that not only thyroid hormone but also thyroid-stimulating hormone (TSH)/TSHR are involved in the expression mechanism of UCP-1 in mouse brown adipose tissue. TSH stimulates thermogenesis and functions to protect a further decrease in body temperature in the hypothyroid state.

Raising at thermoneutrality prevents obesity and hyperphagia in BAT-ablated transgenic mice

1997 ◽  
Vol 272 (4) ◽  
pp. R1088-R1093 ◽  
Author(s):  
A. Melnyk ◽  
M. E. Harper ◽  
J. Himms-Hagen
Keyword(s):  
Adipose Tissue ◽  
Transgenic Mice ◽  
Uncoupling Protein ◽  
Brown Adipocyte ◽  
Specific Expression ◽  
White Adipocyte ◽  
Adipose Tissue Depots ◽  
Brown Adipose ◽  
A Chain ◽  
And Control

Transgenic mice with ablation of brown adipocytes induced by brown adipocyte-specific expression of diphtheria toxin A chain (DTA) driven by the uncoupling protein (UCP) promoter (UCP-DTA mice) become obese and hyperphagic (Lowell, B. B., V. S. Susulic, A. Hamann, J. A. Lawitts, J. Himms-Hagen, B. B. Boyer, L. P. Kozak, and J. S. Flier. Nature 366: 740-742, 1993). A deficit in energy expenditure for brown adipose tissue (BAT) thermogenesis in these mice is presumed to contribute to the development of obesity. The objective of the present study was to obviate any deficit in BAT thermogenesis by raising transgenic and control mice at thermoneutrality (35 degrees C), where both would have equally inactive BAT, to see whether this would prevent the obesity and the hyperphagia. Transgenic and control mice were raised from weaning (3 wk of age) to 8 wk of age at either 24 or 35 degrees C. Raising at 35 degrees C completely prevented development of obesity of UCP-DTA mice, as indicated by their normal carcass fat, normal weights of four major white adipose tissue depots, and normal size of white adipocytes. As seen before, transgenic mice raised at 24 degrees C had excess weight gain by 6 wk of age and by 8 wk had doubled carcass fat, an obesity characterized by increased white adipocyte size with no increase in number of adipocytes. The treatment also prevented hyperphagia of UCP-DTA mice, consistent with the hypothesized role of BAT thermogenesis in control of thermoregulatory feeding (Himms-Hagen, J. Proc. Soc. Exp. Biol. Med. 208: 159-169, 1995). UCP-DTA mice thus differ from genetically obese mice (ob/ob, db/db) for which raising at thermoneutrality is known not to prevent either the obesity or the hyperphagia. Both the obesity and the hyperphagia of UCP-DTA mice appear to be due to their deficit in BAT thermogenesis.

scholarly journals Thermogenesis in Adipose Tissue Activated by Thyroid Hormone

2020 ◽  
Vol 21 (8) ◽  
pp. 3020 ◽  
Author(s):  
Winifred W. Yau ◽  
Paul M. Yen
Keyword(s):  
Adipose Tissue ◽  
Thyroid Hormone ◽  
Body Temperature ◽  
Uncoupling Protein ◽  
Adrenergic Stimulation ◽  
Adipose Tissues ◽  
Adaptive Thermogenesis ◽  
Brown Adipose ◽  
Ucp1 Expression ◽  
Independent Effects

Thermogenesis is the production of heat that occurs in all warm-blooded animals. During cold exposure, there is obligatory thermogenesis derived from body metabolism as well as adaptive thermogenesis through shivering and non-shivering mechanisms. The latter mainly occurs in brown adipose tissue (BAT) and muscle; however, white adipose tissue (WAT) also can undergo browning via adrenergic stimulation to acquire thermogenic potential. Thyroid hormone (TH) also exerts profound effects on thermoregulation, as decreased body temperature and increased body temperature occur during hypothyroidism and hyperthyroidism, respectively. We have termed the TH-mediated thermogenesis under thermoneutral conditions “activated” thermogenesis. TH acts on the brown and/or white adipose tissues to induce uncoupled respiration through the induction of the uncoupling protein (Ucp1) to generate heat. TH acts centrally to activate the BAT and browning through the sympathetic nervous system. However, recent studies also show that TH acts peripherally on the BAT to directly stimulate Ucp1 expression and thermogenesis through an autophagy-dependent mechanism. Additionally, THs can exert Ucp1-independent effects on thermogenesis, most likely through activation of exothermic metabolic pathways. This review summarizes thermogenic effects of THs on adipose tissues.

Role of bone morphogenetic protein 4 in the differentiation of brown fat-like adipocytes

2014 ◽  
Vol 306 (4) ◽  
pp. E363-E372 ◽  
Author(s):  
Ruidan Xue ◽  
Yun Wan ◽  
Shuo Zhang ◽  
Qiongyue Zhang ◽  
Hongying Ye ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Uncoupling Protein ◽  
Brown Fat ◽  
Brown Adipocyte ◽  
White Adipocyte ◽  
Brown Adipose ◽  
And Function ◽  
Brown Adipogenesis

There are two different types of fat present in mammals: white adipose tissue, the primary site of energy storage, and brown adipose tissue, which is specializes in energy expenditure. Factors that specify the developmental fate and function of brown fat are poorly understood. Bone morphogenic proteins (BMPs) play an important role in adipogenesis. While BMP4 is capable of triggering commitment of stem cells to the white adipocyte lineage, BMP7 triggers commitment of progenitor cells to a brown adipocyte lineage and activates brown adipogenesis. To investigate the differential effects of BMPs on the development of adipocytes, C3H10T1/2 pluripotent cells were pretreated with BMP4 and BMP7, followed by different adipogenic induction cocktails. Both BMP4 and BMP7 unexpectedly activated a full program of brown adipogenesis, including induction of the brown fat-defining marker uncoupling protein-1 (UCP1), increasing the expression of early regulators of brown fat fate PRDM16 (PR domain-containing 16) and induction of mitochondrial biogenesis and function. Implantation of BMP4-pretreated C3H10T1/2 cells into nude mice resulted in the development of adipose tissue depots containing UCP1-positive brown adipocytes. Interestingly, BMP4 could also induce brown fat-like adipocytes in both white and brown preadipocytes, thereby decreasing the classical brown adipocyte marker Zic1 and increasing the recently identified beige adipocyte marker TMEM26. The data indicate an important role for BMP4 in promoting brown adipocyte differentiation and thermogenesis in vivo and in vitro and offers a potentially new therapeutic approach for the treatment of obesity.

Brown fat-specific mitochondrial uncoupling protein in adipose tissues of newborn reindeer

1991 ◽  
Vol 260 (6) ◽  
pp. R1229-R1234 ◽  
Author(s):  
P. Soppela ◽  
M. Nieminen ◽  
S. Saarela ◽  
J. S. Keith ◽  
J. N. Morrison ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Adipose Tissue ◽  
Uncoupling Protein ◽  
Brown Fat ◽  
Mitochondrial Uncoupling ◽  
Molecular Weight Characteristic ◽  
Adipose Tissues ◽  
Mitochondrial Uncoupling Protein ◽  
Brown Adipose ◽  
Adverse Weather

Reindeer inhabit a severe arctic or subarctic environment, with the young born in early spring under adverse weather conditions. The extreme northern climate imposes a major thermal challenge to the newborn, and in the present study we have examined fetal, neonatal, and young (from 2 wk before birth to 16 mo postpartum) semidomesticated reindeer from northern Finland for the presence of thermogenic brown adipose tissue. Adipose tissues were removed, mitochondria were prepared, and the proteins were separated by molecular weight and blotted onto nitrocellulose membranes. The membranes were then probed for the presence of the 32,000-relative molecular weight mitochondrial uncoupling protein (UCP) unique to brown fat by use of a rabbit anti-(ground squirrel UCP) serum. Immunoreactivity at the molecular weight characteristic of UCP was present in perirenal, abdominal, inter(pre)scapular, sternal, intralumbar, vertebral, tracheal, inguinal, and omental-mesenteral adipose tissues of newborn reindeer (0-2 days of age). No immunoreactivity was detected in coronary adipose tissue. UCP was found at high levels in interscapular and perirenal adipose tissues of fetal reindeer at 2 wk before birth. Although the protein was present during the first few days postpartum, little immunoreactivity was found at 1 mo of age, and none was evident by 2 mo. UCP and its mRNA were also apparent in perirenal adipose tissue of the newborn of another species of Cervidae, the red deer. It is concluded, on the basis of the immunologic identification of UCP, that most adipose tissues of newborn reindeer represent functional brown fat but that there is a subsequent conversion to white adipose tissue by the 2nd mo of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Invited Review: Uncoupling proteins and thermoregulation

2002 ◽  
Vol 92 (5) ◽  
pp. 2187-2198 ◽  
Author(s):  
George Argyropoulos ◽  
Mary-Ellen Harper
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Uncoupling Protein ◽  
Biochemical Properties ◽  
Atp Production ◽  
Metabolic Functions ◽  
Mitochondrial Inner Membrane ◽  
Brown Adipose ◽  
Total Body ◽  
Body Energy

Energy balance in animals is a metabolic state that exists when total body energy expenditure equals dietary energy intake. Energy expenditure, or thermogenesis, can be subcategorized into groups of obligatory and facultative metabolic processes. Brown adipose tissue (BAT), through the activity of uncoupling protein 1 (UCP1), is responsible for nonshivering thermogenesis, a major component of facultative thermogenesis in newborn humans and in small mammals. UCP1, found in the mitochondrial inner membrane in BAT, uncouples energy substrate oxidation from mitochondrial ATP production and hence results in the loss of potential energy as heat. Mice that do not express UCP1 (UCP1 knockouts) are markedly cold sensitive. The recent identification of four new homologs to UCP1 expressed in BAT, muscle, white adipose tissue, brain, and other tissues has been met by tremendous scientific interest. The hypothesis that the novel UCPs may regulate thermogenesis and/or fatty acid metabolism guides investigations worldwide. Despite several hundred publications on the new UCPs, there are a number of significant controversies, and only a limited understanding of their physiological and biochemical properties has emerged. The discovery of UCP orthologs in fish, birds, insects, and even plants suggests the widespread importance of their metabolic functions. Answers to fundamental questions regarding the metabolic functions of the new UCPs are thus pending and more research is needed to elucidate their physiological functions. In this review, we discuss recent findings from mammalian studies in an effort to identify potential patterns of function for the UCPs.

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