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At least 127 records · Page 7Linked to original sources

PubMed1995

The effect of adipose cell size on the measurement of GLUT 4 in white adipose tissue of obese mice.

Glucose transporter (GLUT 4) was assessed in subcellular membrane fractions of white adipose tissue (WAT) from obese insulin-resistant aurothioglucose (AuTG)- or monosodium glutamate (MSG)-treated mice. Obesity was demonstrated by increased body weight and/or Lee index, as well as by the heavier WAT and brown adipose tissue in relation to similar weights of gastrocnemius and heart. In vivo insulin-resistance in obese animals was suggested by moderate hyperglycemia and severe hyperinsulinemia. Morphological analyses of adipose cells showed a > 10-fold increase in cell volume of obese mice. Subcellular fractionation indicated a reduced (P < 0.01) protein membrane content in the fat-free extract (FFE) from obese mice. However, the specific activity of 5'nucleotidase, a plasma membrane (PM) marker, in FFE and PM did not differ among groups. In addition, the total PM enzyme activity per unit of cell surface area was also unchanged. The GLUT 4 content, assessed by Western blotting and expressed per microgram membrane protein, was reduced by approximately 50% (P < 0.01) in all membrane fractions from obese animals. However, the total FFE GLUT 4 content per cell was increased (P < 0.01), from 23.5 +/- 1.8 in controls to 62.4 +/- 7.6 and 47.4 +/- 5.9 cpm cell-1 10(-3) in AuTG and MSG, respectively, but the total PM GLUT 4 content per unit of cell surface area was highly reduced (P < 0.01), from 165.1 +/- 16.7 in controls to 53.8 +/- 10.9 and 32.0 +/- 5.3 cpm microns-2 10(-9) in AuTG and MSG, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

PubMed1996

Relationship between adipose stromal-vascular cells and adipocytes in human adipose tissue.

OBJECTIVE: To determine the relative amounts of RNA and DNA from adipocytes and adipose stromal-vascular cells to better assess differential gene expression for estrogen receptor and cytochrome P450 aromatase in the two cell fractions of adipose tissue. STUDY DESIGN: Colorimetric and fluorometric assays were used to measure total RNA and DNA, and the relative cell numbers as well as the relative contribution of RNA from adipocytes and stromal-vascular cells were assessed. RESULTS: Adipocytes and stromal-vascular cells exist in a ratio of 2/1. RNA/DNA ratios are the same in the two cell fractions. CONCLUSION: In human subcutaneous adipose tissue, adipocytes are twice as numerous as stromal-vascular cells. The overall transcriptional activity of the cell types appears similar.

Adipocytes↗

PubMed1998

Differential regulation of mouse uncoupling proteins among brown adipose tissue, white adipose tissue, and skeletal muscle in chronic beta 3 adrenergic receptor agonist treatment.

Uncoupling proteins (UCPs) are inner mitochondrial membrane transporters that dissipate the proton gradient, releasing stored energy as heat, without coupling to other energy-consuming processes. Therefore, the UCPs are thought to be important determinants of the metabolic efficiency. To elucidate relationships between the UCPs expressions and insulin sensitivity improvement, we treated KK-Ay mice with beta 3 adrenergic receptor agonist for 21 days and examined the changes of the UCPs mRNA expressions in various tissues. Chronic treatment of a specific beta 3 adrenergic receptor agonist, CL316,243 (0.2 mg/kg body weight/day s.c.) markedly increased the expressions of uncoupling protein 1 (UCP1), uncoupling protein 2 (UCP2), and uncoupling protein 3 (UCP3) by 14-fold, 6-fold, and 16-fold, respectively, in the brown adipose tissue (BAT). The UCP1 and UCP3 mRNA expressions in the white adipose tissue (WAT) were also increased by 12-fold and 9-fold, respectively, but the UCP2 mRNA expression was not changed in this tissue. Interestingly, the UCP2 and UCP3 mRNA expressions were strikingly decreased in the skeletal muscle and heart. Particularly, the UCP3 mRNA expression level in the skeletal muscle was dropped to 10% of that of the saline-treated control mice, indicating that the UCPs mRNA expressions are regulated in tissue-specific ways. The concentrations of plasma insulin and circulating free fatty acid (FFA) were significantly decreased, suggesting that they correlate with the reductions of the UCP2 and UCP3 mRNA expressions in the skeletal muscle and heart. It has been thought that the UCP1 and UCP3 mRNA expressions in the BAT and WAT are mainly controlled by the hypothalamus via the sympathetic nervous system, while the levels of insulin, FFA or both may play important roles in the control of the UCP2 and UCP3 mRNA expressions in the skeletal muscle an heart.

Adipose Tissue↗

PubMed2001

Regulation of UCP1, UCP2, and UCP3 mRNA expression in brown adipose tissue, white adipose tissue, and skeletal muscle in rats by estrogen.

The effects of ovariectomy (OVX) and estrogen substitution on body weight, body composition, food intake, weight gain, and expression of uncoupling proteins (UCPs) in brown adipose tissue (BAT), white adipose tissue (WAT), and skeletal muscle were studied in four groups of rats: (1) Sham-operated rats (N = 8), (2) ovariectomized rats (OVX - E) (N = 8), (3) estrogen-treated OVX rats (OVX + E) (N = 8), and (4) OVX rats on energy restriction (OVX - E + D) (N = 8). OVX was associated with an increase in food intake and body weight gain during a 5-week study period compared to sham-operated rats. The estrogen-substituted rats had a significantly lower food intake and weight gain during the 5 weeks compared to the sham-operated group. However, we also included a nontreated OVX group that was allowed to eat only enough chow to match the weight gain of the sham-operated group. To match the weight gain in the two groups, the OVX group had to consume 16% less chow than the sham-operated group. In BAT, the UCP1 expression was significantly lower in estrogen-deficient rats compared to either intact rats or estrogen-substituted rats, whereas UCP2 and UCP3 mRNA expression was similar in BAT from all four groups. In WAT, both estrogen-deficient groups had significantly lower UCP2 mRNA expression compared to the control rats and estrogen-treated rats; In contrast, the UCP3 mRNA expression in WAT was similar in all four groups. Finally, in skeletal muscle the OVX group on mild energy restriction had reduced UCP3 mRNA expression compared to control, OVX, and estrogen-treated rats. In contrast, the UCP2 mRNA expression in skeletal muscle was similar in all four groups. Thus, the findings that estrogen deficiency is followed by reduced UCP1 expression in BAT and reduced UCP2 expression in WAT in association with weight gain probably caused by a decrease in energy expenditure might indicate that UCPs play a role for the estrogen-mediated changes in body weight and energy expenditure.

Adipose Tissue↗

PubMed1988

The influence of starvation and natural refeeding on the rate of triacylglycerol/fatty acid substrate cycling in brown adipose tissue and different white adipose sites of the rat in vivo. The role of insulin and the sympathetic nervous system.

Triacylglycerol/fatty acid substrate cycling was measured in vivo in brown adipose tissue (BAT) and white adipose tissue (WAT) of fed, starved and refed rats. Starvation (24h) significantly decreased the rate of cycling in BAT, and refeeding chow diet led to a rapid, 6-fold increase in cycling. Cycling rate in WAT was much lower than in BAT, and was not influenced by fasting or refeeding. Similar rates of cycling were found in epididymal, mesenteric, subcutaneous, and scapular WAT depots. Sympathetic denervation of interscapular BAT abolished the response of the tissue to refeeding, as did acute suppression of insulin secretion. Similarly, rats fasted for 3 days showed no acute increase in the activity of the cycle following refeeding.

Adipose Tissue↗

PubMed1996

Expression of c-erbA alpha, c-erbA beta and Rev-erbA alpha mRNA during the conversion of brown adipose tissue into white adipose tissue.

The levels of mRNA encoding uncoupling protein (UCP), thyroid hormone receptors (c-erbA alpha, c-erbA beta) and a related protein Rev-erbA alpha have been studied in brown (pericervical) and white (perirenal) rabbit adipose tissues from birth to 180 days. The c-erbA alpha and c-erbA beta genes are expressed at similar levels in the two tissues. The alpha 1, alpha 2 and beta 1 transcripts do not change notably during development or during the conversion from brown to white phenotype which occurs in pericervical during postnatal life. Rev-erbA alpha mRNA is barely detectable at birth and dramatically increases between 7 and 30 days. However, this increase is not tissue-specific and is also observed in liver and heart. In conclusion, our results show that the decline in UCP expression during the transition from brown to white phenotype cannot be related to changes in the profiles of thyroid hormone receptors or Rev-erbA alpha mRNA expression. These profiles are not different between adipose tissue sites which are brown or white at birth.

Adipose Tissue↗

PubMed1989

Changes in the lipogenic response to feeding of liver, white adipose tissue and brown adipose tissue during the development of obesity in the gold-thioglucose-injected mouse.

Lipogenic response to feeding was measured in vivo in liver, epididymal white adipose tissue (WAT) and interscapular brown adipose tissue (BAT), during the development of obesity in gold-thioglucose (GTG)-injected mice. The fatty acid synthesis after a meal was higher in all tissues of GTG-treated mice on a total-tissue basis, but the magnitude of this increase varied, depending on the tissue and the time after the initiation of obesity. Lipogenesis in BAT from GTG mice was double that of control mice for the first 2 weeks, but subsequently decreased to near control values. In WAT, lipogenesis after feeding was highest 2-4 weeks after GTG injection, and in liver, lipid synthesis in fed obese mice was greatest at 7-12 weeks after the induction of obesity. The post-prandial insulin concentration was increased after 2 weeks of obesity, and serum glucose concentration was higher in fed obese mice after 4 weeks. These results indicate that increased lipogenesis in GTG-injected mice may be due to an increase in insulin concentration after feeding and that insulin resistance (assessed by lipogenic response to insulin release) is apparent in BAT before WAT and liver.

Adipose Tissue↗

PubMed2001

Leptin selectively reduces white adipose tissue in mice via a UCP1-dependent mechanism in brown adipose tissue.

We tested the hypothesis that leptin, in addition to reducing body fat by restraining food intake, reduces body fat through a peripheral mechanism requiring uncoupling protein 1 (UCP1). Leptin was administered to wild-type (WT) mice and mice with a targeted disruption of the UCP1 gene (UCP1 deficient), while vehicle-injected control animals of each genotype were pair-fed to each leptin-treated group. Leptin reduced the size of white adipose tissue (WAT) depots in WT mice but not in UCP1-deficient animals. This was accompanied by a threefold increase in the amount of UCP1 protein and mRNA in the brown adipose tissue (BAT) of WT mice. Leptin also increased UCP2 mRNA in WAT of both WT and UCP1-deficient mice but increased UCP2 and UCP3 mRNA only in BAT from UCP1-deficient mice. These results indicate that leptin reduces WAT through a peripheral mechanism requiring the presence of UCP1, with little or no involvement of UCP2 or UCP3.

Adipose Tissue↗

PubMed1986

Modulation of fatty acid synthesis in vivo in brown adipose tissue, liver and white adipose tissue of cold-acclimated rats.

The present experiment was an appraisal of the relative importance of fatty acid synthesis in brown adipose tissue (BAT) in young 28 or 5 degrees C adapted rats (9 weeks old). With a low-fat diet in vivo incorporation of 3H2O into BAT fatty acids was 8 times lower during the day than during the night and was not modified by a 6-hour fast during the day (28 degrees C). Cold acclimation doubled (night) or increased 8 times (day) BAT lipogenesis. Fasting led to a halving of the diurnal rate. A high-fat diet led to large decrease in synthesis rate during the night but had a weak effect on diurnal synthesis. The specific activity of fatty acids was 3 times lower in phospholipids than in neutral lipids. A comparison between 9- and 15-week-old rats indicated that in older warm-adapted rats BAT lipogenesis decreased by half but that cold stimulation was unaltered. These results were compared with hepatic and epididymal white adipose tissue lipogenesis. In conclusion, we showed that BAT of 5 degrees C rats is an important but not the major site for the conversion of carbohydrate to fat and that the proportional involvement of each tissue is age-dependent.

Acclimatization↗

PubMed1987

Adipose tissue development: the role of precursor cells and adipogenic factors. Part I: Adipose tissue development and the role of precursor cells.

Obesity is regarded as a heterogeneous syndrome, which may appear in different forms. Various causes have been found to contribute to its pathogenesis. During recent years investigations of adipose tissue cellularity and its dynamic changes have gained growing interest. An important progress was the discovery of adipose tissue precursor cells. These cells have not yet been precisely identified by morphological and biochemical methods in intact tissue. However, due to methodological developments such precursor cells can be cultured both as primary cultures and as established cell lines. These culture systems have proven to be valuable models for the study of the processes involved in the formation of new fat cells.

Adipose Tissue↗

PubMed1992

Effect of adipose tissue site, animal size, and fasting on lipolysis in bovine adipose tissue in vitro.

1. Lipolytic rates expressed as mumol glycerol released per mg protein increased with body weight in Holstein steers. 2. Lipolytic rates were greatest in both inner and outer back fat and lowest in omental, perirenal, and intermuscular fat depots. 3. Epinephrine stimulated overall glycerol release 3-5-fold. 4. Fasting resulted in greater basal lipolytic rates but epinephrine-stimulated rates tended to be greater for nonfasted steer adipose tissue. 5. Lipolytic activity in adipose tissue seems to increase with growth and fattening, and differences in lipolytic rates between various depots diminish with growth.

Adipose Tissue↗

PubMed2003

Paracrine relationships between adipose and lymphoid tissues: implications for the mechanism of HIV-associated adipose redistribution syndrome.

The adipocytes anatomically associated with lymph nodes and omental milky spots have site-specific properties that equip them to interact locally with lymphoid cells. Paracine provisioning of peripheral immune responses improves their efficiency and emancipates activated lymphocytes from competition with other tissues for blood-borne nutrients. Prolonged disruption to such paracine interactions might contribute to the HIV-associated adipose redistribution syndrome, causing selective hypertrophy of the mesentery, omentum and other lymphoid tissue-containing adipose depots, while nodeless depots atrophy.

Adipose Tissue↗

PubMed1970

Structure-function relationships in the adipose cell. 3. Effects of bovine serum albumin on the metabolism of glucose and the release of nonesterified fatty acids and glycerol by the isolated adipose cell.

Serum albumin stimulates the uptake of U-glucose-(14)C and the incorporation of (14)C-counts into triglyceride glycerol and inhibits the incorporation of (14)C-counts into triglyceride fatty acids by isolated adipose cells; insulin and epinephrine enhance these effects. In the absence of hormones, these responses to albumin increase with increasing albumin concentration. In the presence of insulin, a qualitatively similar pattern of increasing responses to albumin is observed; the enhancement of each response by insulin is, however, only slightly potentiated by higher albumin concentrations. In contrast, in the presence of epinephrine, these responses to albumin are maximal at the lowest albumin concentration tested, 0.1%; the enhancement of each response by epinephrine is similarly maximal at 0.1% albumin, but decreases rapidly as the albumin concentration is raised. Increasing serum albumin concentrations do, however, stimulate the release of fatty acids and glycerol by epinephrine-treated cells increasingly until a plateau, determined by the epinephrine dose, is reached. These data support the suggestion that intracellular fatty acid levels function in the regulation of adipose cell activity, and further suggest that serum albumin plays a role in determining the metabolic fate of these fatty acids.

Adipose Tissue↗

PubMed2003

Efficient proliferation and adipose differentiation of human adipose tissue-derived vascular stromal cells transfected with basic fibroblast growth factor gene.

Human vascular stromal (VS) cells obtained from mature adipose tissue were transfected with an adenovirus vector carrying the basic fibroblast growth factor (bFGF) gene. bFGF protein was observed in VS cell nuclei 24 h after transfection and in the cytoplasm and extracellular space 72 h after transfection. Naive VS cells were almost static in vitro and proliferated in a dose-dependent manner on stimulation with recombinant bFGF (rbFGF). However, bFGF-transfected VS cells proliferated spontaneously to the same extent as naive VS cells when stimulated with rbFGF at 100 ng/ml. The former cells started to proliferate on day 3 after transfection and the proliferation pattern was similar to that of the latter cells, although only a slight amount of bFGF protein was detected in the culture medium when the bFGF-transfected cells started to proliferate. The proliferation of bFGF-transfected VS cells was completely inhibited by bFGF neutralizing antibody, which also completely inhibited the proliferation of naive VS cells stimulated with rbFGF. Under conditions favoring differentiation to adipocytes, bFGF-transfected VS cells stopped proliferating and started to accumulate lipid in the cytoplasm. bFGF-transfected VS cells, which spontaneously and efficiently proliferate while preserving their ability to differentiate into adipocytes, may be an adequate cell source for human adipose tissue regeneration.

Adipose Tissue↗

PubMed2005

White adipose tissue sensory nerve denervation mimics lipectomy-induced compensatory increases in adiposity.

The sensory innervation of white adipose tissue (WAT) is indicated by the labeling of sensory bipolar neurons in the dorsal root ganglion after retrograde dye placement into WAT. In addition, immunoreactivity (ir) for sensory-associated neuropeptides such as calcitonin gene-related peptide (CGRP) and substance P in WAT pads also supports the notion of WAT sensory innervation. The function of this sensory innervation is unknown but could involve conveying the degree of adiposity to the brain. In tests of total body fat regulation, partial surgical lipectomy triggers compensatory increases in the mass of nonexcised WAT, ultimately resulting in restoration of total body fat levels in Siberian hamsters and other animals. The signal that triggers this compensation is unknown but could involve disruption of WAT sensory innervation that accompanies lipectomy. Therefore, a local and selective sensory denervation was accomplished by microinjecting the sensory nerve neurotoxin capsaicin bilaterally into epididymal WAT (EWAT) of Siberian hamsters, whereas controls received vehicle injections. Additional hamsters had bilateral EWAT lipectomy (EWATx) or sham lipectomy. As seen previously, EWATx resulted in significantly increased retroperitoneal WAT (RWAT) and inguinal WAT (IWAT) masses. Capsaicin treatment significantly decreased CGRP- but not tyrosine hydroxylase-ir, attesting to the diminished and selective sensory innervation. Capsaicin-treated hamsters also had increased RWAT and, to a lesser degree, IWAT mass largely mimicking the WAT mass increases seen after lipectomy. Collectively, these data suggest the possibility that information related to peripheral lipid stores may be conveyed to the brain via the sensory innervation of WAT.

Adaptation, Physiological↗

PubMed1991

Differential regulation of adipose tissue glucose transporters in genetic obesity (fatty rat). Selective increase in the adipose cell/muscle glucose transporter (GLUT 4) expression.

Adipocytes from young obese Zucker rats exhibit a hyperresponsive insulin-mediated glucose transport, together with a marked increase in cytochalasin B binding as compared with lean rat adipocytes. Here, we examined in these cells the expression of two isoforms of glucose transporter, the erythroid (GLUT 1) and the adipose cell/muscle (GLUT 4) types, in rats aged 16 or 30 d, i.e., before and after the emergence of hyperinsulinemia. GLUT 1 protein and mRNA levels were identical in the two genotypes at both ages. In contrast, the levels of GLUT 4 protein in obese rat adipocytes were 2.4- and 4.5-fold those of lean littermates at 16 and 30 d of age, respectively, in perfect agreement with the genotype effect on insulin-stimulated glucose transport activity. The levels of GLUT 4 mRNA per fat pad were increased 2.3- and 6.2-fold in obese vs. lean rats 16- and 30-d-old, indicating a pretranslational level of regulation. The obese phenotype was not associated with overexpression of GLUT 4 mRNA in gastrocnemius muscle. This work indicates that the fa gene exerts a differential control on the expression of GLUT 1 and GLUT 4 in adipose tissue and provides evidence that independent of hyperinsulinemia, genotype is a major regulatory factor of GLUT 4 expression in this tissue.

Adipose Tissue↗

PubMed2001

Angiotensin II as a trophic factor of white adipose tissue: stimulation of adipose cell formation.

White adipose tissue is known to contain the components of the renin-angiotensin system giving rise to angiotensin II (AngII). In vitro, prostacyclin is synthesized from arachidonic acid through the activity of cyclooxygenases 1 and 2 and is released from AngII-stimulated adipocytes. Prostacyclin, in turn, is able to favor adipocyte formation. Based upon in vivo and ex vivo experiments combined to immunocytochemical staining of glycerol-3-phosphate dehydrogenase (GPDH), an indicator of adipocyte formation, it is reported herein that AngII favors the appearance of GPDH-positive cells. In the presence of a cyclooxygenase inhibitor, this adipogenic effect is abolished, whereas that of (carba)prostacyclin, a stable analog of prostacyclin that bypasses this inhibition, appears unaltered. Taken together, these results are in favor of AngII acting as a trophic factor implicated locally in adipose tissue development. It is proposed that AngII enhances the formation of GPDH-expressing cells from preadipocytes in response to prostacyclin released from adipocytes.

Adipocytes↗

PubMed2005

Excess visceral and hepatic adipose tissue in Turner syndrome determined by magnetic resonance imaging: estrogen deficiency associated with hepatic adipose content.

Obesity, predominantly centrally distributed, is common in women with Turner syndrome (TS) and is thought to contribute to the increased risk of atherosclerosis; however, insulin concentrations are unexpectedly low. To explore this discrepancy, we assessed fat content and distribution by magnetic resonance imaging (MRI) and bioelectrical impedance (BI). Six nondiabetic, estrogen-treated women with TS were compared with six age-matched normal controls of similar body mass index. Clinical history, anthropometric measurements, biochemical markers, and MRI and BI measures of adiposity were assessed. TS women had increased intrahepatocellular lipids (IHCL) on MRI. After height adjustment, they also had an excess of total and visceral compared with sc adipose tissue (AT) than controls, without elevated insulin concentrations. BI and MRI measures correlated strongly for total and sc, but not visceral, AT in TS. IHCL was associated with cumulative estrogen-deficient years (r = 0.928; P = 0.008). Women with TS depart from the classical picture of metabolic syndrome despite an excess of total and visceral AT on MRI. Elevated IHCL in TS is associated with estrogen deficiency. BI may be useful to estimate total body fat, but does not reliably localize fat depots in TS.

Adipose Tissue↗