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At least 91 records · Page 5Linked to original sources
PubMed2001

Role of the 4G/5G polymorphism of PaI-1 gene promoter on PaI-1 levels in obese patients: influence of fat distribution and insulin-resistance.

As PAI-1, a cardiovascular risk factor linked to insulin-resistance, may be influenced by a 4G/5G gene polymorphism in disease states, we studied both PAI-1 plasma concentration (PAI-1:Ag) and 4G/5G polymorphism, and their relationship with anthropometric and endocrinemetabolic parameters in 93 obese patients and 79 lean normal subjects. In obese patients PAI-1:Ag levels were significantly increased, namely in males and in those with central obesity, and tightly related to the insulin-resistance parameters. In obese patients the 4G/5G polymorphism was a determinant of PAI-1:Ag levels, which were highest in 4G/4G, intermediate in 4G/5G and lowest in 5G/5G genotype carriers. PAI-1:Ag levels were significantly associated with most of anthropometric and endocrine-metabolic parameters only in 4G allele obese carriers. Moreover, only in patients with central obesity was the relationship between genotype and PAI-1 concentration maintained, with the highest levels in the 4G/4G patients. In each genotype subset of patients with central, but not peripheral, obesity PAI-1:Ag levels were significantly increased compared to their lean counterparts. In conclusion, the 4G/5G polymorphism may influence PAI-1 expression in obesity, with a crucial role in central but not peripheral adiposity. Since subjects with central obesity are at high risk for cardiovascular disease, the effects of the 4G/5G polymorphism on PAI-1 concentration may further enhance this risk.

Adult↗
PubMed2003

Cardiovascular consequences of obesity.

Obesity is a problem of epidemic proportions that is associated with adverse cardiovascular outcomes. The long-term efficacy of currently available treatments is limited, and therapeutic benefits might paradoxically be achieved only at the expense of other serious adverse cardiovascular consequences. Owing to these limitations, new paradigms in the management of obesity are being explored, including expanded surgical and pharmacologic therapies. Recent discoveries in the pathogenesis of obesity, including the discovery of leptin, might lead to new treatment options. Leptin dysregulation within the central nervous system or in peripheral adipose tissue has a putative role in the pathogenesis of obesity. Furthermore, important differences exist between men and women in regard to leptin levels; these discrepancies might ultimately impact the therapeutic approach in a gender-specific manner. The goals of obesity therapy and the appropriate therapeutic endpoints are being evaluated to maximize the efficacy of therapy and improve cardiovascular outcomes, while diminishing the risk of adverse cardiovascular complications.

Anti-Obesity Agents↗
PubMed1989

Cellular composition of rat bone marrow stroma. Antigen-defined subpopulations.

Although stromal cells establish the architecture of mammalian bone marrow and organize hemopoiesis, the interrelationships among their macrophage, fibroblastic, endothelial, and adipocyte-like components are not wholly understood. Using murine monoclonal antibodies to cultured adherent cells of rat bone marrow, we observed that the predominant fibroblastoid cells grown from marrow differed from those of non-hemopoietic organs. The marrow type bore a detectable quantity of the ST3 but not ST4 antigen, whereas those from lung, diaphragm, and epididymal fat pad, bore more ST4 than ST3. Those from spleen were an equal mix of both types. Although the tissue distribution of the ST3 antigen was similar to that of Thy-1, it was not identical, and in the brain, the two structures were localized in different areas. While none of the ST3, ST4 (fibroblast directed), or BN(MB)35 (myeloid directed) antibodies recognized fat cells cultured from marrow, the ST10 antibody, selected for binding to marrow derived fat cells, stained peripheral adipose cells, unidentified aglobular cells in areas of fat cell formation, and macrophages, but not fibroblasts. On the basis of these observations, we suggest that the fibroblastoid cells of the marrow are different from those of non-hemopoietic tissues.

Adipose Tissue↗
PubMed1985

[Insulin receptors in fat tissue of human and rat during pregnancy].

Insulin receptors in fat cell membranes (10(5)g pellets) were investigated by a conventional incubation method in pregnant and nonpregnant rats or women. Insulin binding in pregnant L20 rats was 8.1 +/- 2.1% (M +/- SD) less than that in nonpregnant rats (14.5 +/- 3.5%) in peripheral adipose tissues (p less than 0.05). In the former a reciprocal rise in the serum insulin level was observed. In pregnant women, insulin binding was determined in subcutaneous fat tissues obtained at cesarean section or other laparotomy. Insulin binding was 29.3 +/- 8.9% in nonpregnant women, and it did not change in early pregnancy (34.3 +/- 6.2%, NS). However, it decreased obviously in late pregnancy (20.4 +/- 6.4%) (p less than 0.05). Scatchard analysis indicated that the decrease in insulin binding was due to the changes in the number of insulin receptors in fat cell membranes. Their Kd values were indistinguishable from each other in rats and women. In addition, insulin binding correlated significantly with Insulin Sum, Glucose Sum at 75g OGTT, TG and FFA in serum. These results suggested that insulin receptors in adipose tissues were suppressed in late pregnancy, and this might be the cause of the "insulin resistance" observed in the maternal body in late pregnancy.

Adipose Tissue↗
PubMedDate not supplied

[Lipolysis in fatty tissue of patients with adrenohypercorticism].

Lipolytic activity was studied in subcutaneous and peripheric adipose tissue of patients with adrenohypercorticism (25 patients with Itsenko-Cushing disease and 4 patients with Cushing syndrome caused by corticosteroma of adrenal gland) and in 11 persons without this pathology. The lipolytic activity of the both adipose tissues in the patients with Itsenko-Cushing disease was similar to that of healthy persons and decreased in the patients with Cushing syndrome. The receptor-enzymatic system, responsible for lipolysis in adipose tissue, was not impaired in Itsenko-Cushing disease; differences found in lipolytic effects of corticotropin and somatotropin were caused by deteriorations in secretion of endogenous hormones in the disease. This system was inhibited in Cushing syndrome. Antilipolytic effect of insulin (especially in presence of glucose) was more distinct in subcutaneous adipose tissue of patients with Itsenko-Cushing disease as compared with controls.

Adipose Tissue↗
PubMed2002

[Adipose tissue within peripheral nerves. Study of the human sciatic nerve].

AIM: To describe the distribution of intraneural adipose cells in relation to nerve fascicles in a portion of peripheral nerve usually involved in accomplishing an anesthetic blockade of a lower extremity. METHOD: Using a scanning electron microscope, we studied sciatic nerve samples from the point of amputation of a lower limb of three patients. The samples were obtained at the upper angle of the popliteal fossa, 10-15 cm cephalad to the knee joint line. RESULTS: During dissection of the sciatic nerve samples, we observed a solitary trunk, but examination of the cross-sections under the microscope revealed the components of two clearly separated branches joined by supporting tissue. The sciatic nerve had an oval form in the portion under study, measuring 6.5 to 7.5 mm by 3.6 to 3.9 mm. Between the fascicles, the adipose tissue varied in thickness from 0.5 mm in the central zones to 0.2 mm in the peripheral zones. The adipocytes, which were all similar in the size with diameters of 40 microns, were empty, as a result of elimination of the lipid vacuoles during fixation. The adipose tissue was distributed inside the epineurium to surround isolated fascicles or groups of fascicles. CONCLUSIONS: The adipose tissue inside a nerve surrounded the fascicles to form adipose sheaths that separated the fascicles from one another. The thicknesses of these adipose sheaths varied from one fascicle to another. Cells join to make it possible to create a compact adipose sheet that can delay the diffusion of local anesthetic injected near a nerve and that can therefore interfere with the characteristics of an anesthetic blockade.

Adipose Tissue↗
PubMed1993

Depletion of adipose tissue and peripheral nerve alpha-tocopherol in adult dogs.

To assess the relationship between tissue alpha-tocopherol depletion and histopathologic or functional changes in nervous tissue, a longitudinal study of male 1-year-old beagle dogs, two fed a vitamin E-deficient diet (0.05 +/- 0.02 mg alpha-tocopherol/kg;--E dogs) and two fed a vitamin E-supplemented diet (114 +/- 14 mg alpha-tocopherol/kg; +E dogs), was carried out. Plasma and adipose tissue alpha-tocopherol concentrations, neurological examinations, and sensory and motor nerve conduction velocities were determined at approximately 8-wk intervals over 109 wk. Tibial nerve alpha-tocopherol concentrations were measured at 65 and 109 wk; adjacent sections were examined for histologic changes. In the two -E dogs, plasma alpha-tocopherols declined linearly on a semilog plot to < 0.1 microgram/mL by 109 wk. Plasma alpha-tocopherol concentrations were depleted to half of the initial concentrations in approximately 87 d. Adipose tissue alpha-tocopherol concentrations (based on wet weight, cholesterol or triglyceride) also declined linearly on semilog plots, and were depleted to half of the initial concentrations in approximately 120 d. Tibial nerve alpha-tocopherols (ng/microgram cholesterol) in -E dogs decreased to 16% of average +E at 65 wk, and to 2% at 109 wk. Neurologic examinations, histologies and nerve conduction velocities were normal in all dogs throughout the study. Our results demonstrate in dogs that depletion of plasma, adipose tissue and nerve alpha-tocopherol precedes histologic and functional changes in peripheral nerves during vitamin E deficiency.

Adipose Tissue↗
PubMed1995

Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks.

The recent positional cloning of the mouse ob gene and its human homology has provided the basis to investigate the potential role of the ob gene product in body weight regulation. A biologically active form of recombinant mouse OB protein was overexpressed and purified to near homogeneity from a bacterial expression system. Peripheral and central administration of microgram doses of OB protein reduced food intake and body weight of ob/ob and diet-induced obese mice but not in db/db obese mice. The behavioral effects after brain administration suggest that OB protein can act directly on neuronal networks that control feeding and energy balance.

Animals↗
PubMed2006

Evidence of an oscillating peripheral clock in an equine fibroblast cell line and adipose tissue but not in peripheral blood.

The master mammalian pacemaker in the brain controls numerous diverse physiological and behavioral processes throughout the organism. Timing information is continually transmitted from the master clock to peripheral organs to synchronize rhythmic daily oscillations of clock gene transcripts and control local physiology. To investigate the presence of peripheral clocks in the horse, quantitative real-time RT-PCR assays were designed to detect levels of equine clock genes. Expression profiles for Per2, Bmal1 and Cry1 were first determined in a synchronized equine cell line. Subsequently, expression in equine whole blood and adipose tissue was assessed. Robust circadian oscillations of Per2, Bmal1 and Cry1 were observed in vitro. A synchronized molecular clock was also demonstrated in equine adipose tissue although oscillation of Bmal1 was less robust than that of Per2 and Cry1. In contrast to previous studies in humans and rats however, there was no evidence of synchronized clock gene expression in equine peripheral blood. These studies suggest that synchronous control of clock gene oscillation in equine peripheral blood is not as tightly regulated as in other species and may reflect the influence of different evolutionary challenges modifying the function of a peripheral clock.

Adipose Tissue↗
PubMed1982

A comparative study of steroid concentrations in human adipose tissue and the peripheral circulation.

Using radioimmunological methods, levels of cortisol, dehydroepiandrosterone, androstenedione, testosterone, oestrogens (oestradiol + oestrone), progesterone and 17 alpha-hydroxyprogesterone were determined in adipose tissue and peripheral blood obtained during surgical treatment of patients with non-endocrine diseases. The steroid content of human adipose tissue was observed to be extremely high relative to that in the general circulation, giving a tissue/serum ratio of 0.4 to 13.2. The concentration of steroids decreased in the following order: dehydroepiandrosterone greater than cortisol greater than androstenedione greater than progesterone greater than testosterone greater than 17 alpha-hydroxyprogesterone greater than oestradiol + oestrone. This sequence is different from that found in blood. When anthropometric variables were taken into consideration, the adipose tissue mass of severely obese subjects contained a steroid pool far greater than that in the total blood volume.

Adipose Tissue↗
PubMed2005

Mitochondrial DNA levels of peripheral blood mononuclear cells and subcutaneous adipose tissue from thigh, fat and abdomen of HIV-1 seropositive and negative individuals.

Mitochondrial dysfunction has been demonstrated in subcutaneous adipose tissue from lipoatrophic HIV-1-infected patients treated with nucleoside reverse transcriptase inhibitors (NRTIs). To further assess mitochondrial toxicity, mitochondrial DNA (mtDNA) copies/cell were measured in subcutaneous fat from various sites. Peripheral adipose tissues were obtained from the abdominal wall near the umbilicus, anterior lateral thigh, and dorsal cervical region of the neck of individuals from four cohorts: 1) seven lipoatrophic HIV-1-infected patients receiving a regimen with nucleoside reverse transcriptase inhibitors (NRTIs) as part of highly active antiretroviral therapy (HAART) for > 6 months; 2) seven non-lipoatrophic HIV-1-infected patients receiving NRTIs-containing HAART; 3) five HIV-1-infected patients on antiretroviral therapy < 2 weeks (naive); 4) and five HIV-1-negative participants. Along with the adipose tissue samples, peripheral blood mononuclear cells (PBMC) were also obtained from each patient for mtDNA depletion examination. Total DNA was isolated and mtDNA copies/cell quantitated by competitive and real-time PCR. MtDNA copies/cell in abdomen, thigh, and neck fat were depleted in lipoatrophic HIV-1 seropositive compared to the seropositive naive and seronegative cohorts. MtDNA copies/cell in thigh and neck fat were also decreased in non-lipoatrophic subjects exposed to NRTIs compared with NRTI-naive and HIV seronegative controls. PBMC values did not differ among the cohorts and there was no correlation with lipoatrophy state or HIV-1 serostatus. Additionally, differences in mtDNA copies/cell were observed in the fat depots from seronegative subjects. Thigh fat mtDNA levels were 45-55% lower than abdomen and neck. These studies help demonstrate that mtDNA levels can vary in different subcutaneous adipose depots suggesting possible metabolic differences.

Adipose Tissue↗
PubMed2006

Characterization of peripheral circadian clocks in adipose tissues.

First described in the suprachiasmatic nucleus, circadian clocks have since been found in several peripheral tissues. Although obesity has been associated with dysregulated circadian expression profiles of leptin, adiponectin, and other fat-derived cytokines, there have been no comprehensive analyses of the circadian clock machinery in adipose depots. In this study, we show robust and coordinated expression of circadian oscillator genes (Npas2, Bmal1, Per1-3, and Cry1-2) and clock-controlled downstream genes (Rev-erb alpha, Rev-erb beta, Dbp, E4bp4, Stra13, and Id2) in murine brown, inguinal, and epididymal (BAT, iWAT, and eWAT) adipose tissues. These results correlated with respective gene expression in liver and the serum markers of circadian function. Through Affymetrix microarray analysis, we identified 650 genes that shared circadian expression profiles in BAT, iWAT, and liver. Furthermore, we have demonstrated that temporally restricted feeding causes a coordinated phase-shift in circadian expression of the major oscillator genes and their downstream targets in adipose tissues. The presence of circadian oscillator genes in fat has significant metabolic implications, and their characterization may have potential therapeutic relevance with respect to the pathogenesis and treatment of diseases such as obesity, type 2 diabetes, and the metabolic syndrome.

Adiponectin↗
PubMed1991

Peripheral mechanisms of thermogenesis induced by ephedrine and caffeine in brown adipose tissue.

The peripheral mechanisms by which ephedrine and caffeine influence thermogenesis were investigated in innervated rat interscapular brown adipose tissue (IBAT) by assessing its rate of oxygen consumption (MO2) in vitro. Dose-response measurements with tissues from intact or sympathectomized (6-OHDA) animals indicate that the thermogenic effects of low concentrations of ephedrine and also of caffeine are entirely dependent upon the presence of intact sympathetic nerve endings, and thus depend on presynaptic mechanisms. Direct postsynaptic stimulation of thermogenesis is only apparent at much higher concentrations, namely greater than 1 microM for ephedrine and greater than 2mM for caffeine. At subminimal concentrations that neither ephedrine nor caffeine influenced basal tissue respiration, they induced a 4-5-fold increase in basal MO2 when administered in combination, a synergistic response prevented by pre-treatment of the rat with 6-OHDA. Synergistic increases in IBAT respiration were also obtained when subminimal concentration of ephedrine was added to 3-propylxanthine (a specific inhibitor of phosphodiesterase), to 8-phenyltheophylline (a potent adenosine receptor antagonist) or to adenosine deaminase (for enzymatic inactivation of endogenous adenosine). Conversely, the marked synergism in thermogenic response with ephedrine + caffeine was reduced in the presence of 2-chloroadenosine (an adenosine analogue). In tissues from fasted rats, the ephedrine + caffeine synergism in thermogenic response, although attenuated, was nevertheless present. These studies therefore demonstrate that ephedrine, at doses comparable with therapeutic use, stimulates thermogenesis in BAT via sympathetically released NA. In addition, a synergistic interaction between caffeine and ephedrine on BAT thermogenesis is explained by ephedrine's enhancement of sympathetic neuronal release of NA, together with caffeine's dual ability to antagonize adenosine and to inhibit cellular phosphodiesterase activity.

2-Chloroadenosine↗
PubMedDate not supplied

Neonatal hypothalamic androgenization in the female rat induces changes in peripheral insulin sensitivity and adiposity function at adulthood.

UNLABELLED: It is recognized that there exists a link between hyperandrogenicity and insulin resistance. OBJECTIVE: By using the neonatally androgenized female rat we explored whether this treatment modifies peripheral insulin sensitivity and visceral fat function at adulthood. EXPERIMENTAL DESIGNS: On day 5 of age, female Sprague-Dawley pups were injected, sub cutaneous, with either 50 ml of sterile corn oil alone (CT) or containing 1.25 mg of testosterone propionate (TP) and further used for experimentation on day 100 of age. CT and TP rats were killed by decapitation in non-fasting condition and blood samples were kept frozen for measurement of different metabolites. Immediately after sacrifice, freshly dissected visceral fat pads were used for isolation of adipocytes, these cells were then incubated with medium alone or containing different concentrations of insulin in order to determine leptin secreted into the medium. Additionally, in vivo metabolic responses to intravenous high glucose load were performed in, 24 hour-fasting, CT and TP rats. RESULTS: We found that neonatal androgenization induced adult animals displaying higher visceral adiposity mass, body weight and leptinemia than CT rats. No group differences were found in basal circulating levels of several hormones and metabolic parameters. The results of the high glucose load 90-min test indicated that TP and CT rats developed similar glycemia but this accounted because of an early significantly higher peak values of circulating insulin in TP than in CT rats, regardless of similar enhancement in circulating glucocorticoid concentrations in both groups. While high glucose load significantly increased, over the baseline, circulating leptin concentrations as early as 30 min post-glucose in CT rats, in TP animals, it significantly enhanced leptinemia only by the end of the test. Finally, results of in vitro incubations of isolated visceral adipocytes indicated that cells from androgenized rats spontaneously released more leptin than control cells, although they were less responsive than CT cells to insulin-induced leptin output. CONCLUSION: Our study strongly supports the hypothesis that development of insulin resistance seems to be dependent on early hyperandrogenicity.

Adipocytes↗
PubMed1991

Role of sympathetic nerves in effects of estradiol on rat white adipose tissue.

Two experiments examined the role of the sympathetic nerves in estradiol-induced fat pad weight losses in ovariectomized (OVX) rats. Rats were OVX, and the retroperitoneal white adipose tissue (RWAT) was unilaterally denervated 4 wk later. After 14 days of treatment with estradiol benzoate (EB, 2 micrograms/day), the intact pads lost 23% more weight than the denervated pads. There was no effect of denervation on fat pad weight or on cytosol estrogen receptor concentration in RWAT in the animals treated with sesame oil vehicle. These data suggest that the sympathetic nerves play a role in estrogen-induced reductions in fat pad weight but not via changes in adipose tissue cytosol estrogen receptors. A second experiment examined whether estradiol-induced fat pad weight losses are accompanied by increased norepinephrine (NE) turnover, an index of sympathetic activity, in adipose tissue. Rats were OVX and treated with EB or sesame oil vehicle. NE turnover was assessed by measuring the decline of tissue NE over time after injection of alpha-methyl-p-tyrosine, an inhibitor of tyrosine hydroxylase activity and thus NE biosynthesis. NE turnover in RWAT, but not heart, was significantly greater in animals treated with EB, suggesting that estradiol decreases fat pad weight in part by increasing sympathetic nervous system activity. It is possible that estradiol acts in the brain to regulate the activity of the sympathetic nerves to white adipose tissue and peripherally to alter adipose tissue responsiveness to catecholamines.

Adipose Tissue↗
PubMed1996

The effect of metformin on adipose tissue metabolism and peripheral blood flow in subjects with NIDDM.

OBJECTIVE: To examine the effect of metformin on net lactate and glycerol release in NIDDM subjects, we used abdominal subcutaneous microdialysis combined with 133Xe clearance. Skeletal muscle blood flow (MBF) was assessed simultaneously both before and after metformin treatment. RESEARCH DESIGN AND METHODS: Nine male patients with NIDDM (age 53 +/- 2 years [mean +/- SE]; BMI 30.2 +/- 1.4 kg/m2; body fat 23.0 +/- 2.6 kg; diabetes duration 4.6 +/- 1.5 years; six of nine receiving sulfonylurea treatment) were recruited into an open study. They were studied after an overnight fast, both before and after 1 week of additional treatment with 500 mg metformin three times daily. Nine weight- and age-matched nondiabetic subjects served as a control group. RESULTS: Postabsorptive net subcutaneous lactate release increased (149 +/- 50 vs. 475 +/- 127 nmol.100 g-1.min-1, P < 0.05) whereas plasma lactate was unchanged after metformin treatment in the NIDDM patients. The net decrease of glycerol release 90 min after an oral glucose tolerance test was more pronounced (110 +/- 30 vs. 199 +/- 20 nmol.100 g-1.min-1, P < 0.05) after metformin treatment. Both adipose tissue blood flow (ATBF) (1.5 +/- 0.1 vs. 2.3 +/- 0.2 ml.100 g-1.min-1, P < 0.01) and MBF (3.2 +/- 0.4 vs. 4.2 +/- 0.5 ml.100 ml-1.min-1, P < 0.05) increased after metformin treatment. CONCLUSIONS: In this open study, postabsorptive net lactate release in abdominal subcutaneous adipose tissue was clearly increased in NIDDM patients after metformin treatment. Basal ATBF as well as MBF was improved after metformin treatment. Whether this reflects enhanced metabolic control or is a drug-specific effect remains to be established.

Adipose Tissue↗