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PubMed1995

Body habitus changes among adult males from the normative aging study: relations to aging, smoking history and alcohol intake.

The Normative Aging Study (NAS) recruited 2280 Boston area healthy males aged 21 to 80 in 1961 through 1970. Clinical exams have continued at 3- to 5-year intervals. Obesity was not an exclusion criterion. Stability in weight and body habitus among 867 adult participants in the NAS was evaluated at 5- and 15-year follow-ups. At study entry, age was linearly related to central adiposity [abdominal circumference (AC) and ratio of AC/Hip Breadth (HB)] throughout the entire age range (30 to 78 years) and linearly and quadratically related to weight (WT) and Body Mass Index (BMI) (kg/m2) with maximal values at age 50. Over 15 years, changes in adiposity were strongly related to age; the greatest increases were among those initially 30 to 44 years of age with decrements in several adiposity measures (BMI, AC) only among the oldest subjects (60+ at entry); significant quadratic effects of age for BMI (p < .001), WT (p < .02) and AC (p < .01). There were major secular differences; men born later were heavier and fatter at the same ages as men born earlier. Men who gained (> 1 BMI) were younger while men who lost (> 1 BMI) had greater initial central adiposity than others. Smoking cessation was independently associated with increments in both central and peripheral adiposity. Moderate alcohol intake was associated with lower gains in AC/HB ratios at 15 years compared with little or high consumption. In general, aging was associated with trends towards central adiposity which tended to plateau or decrease at the oldest ages.

Adult↗
PubMed1997

Weaning marginally affects glucose transporter (GLUT4) expression in calf muscles and adipose tissues.

The nutritional regulation of glucose transporter GLUT4 was studied in eight muscles and four adipose tissues from two groups of preruminant (PR) or ruminant (R) calves of similar age (170 d), empty body weight (194 kg) at slaughter, and level of net energy intake from birth onwards. Isocitrate dehydrogenase (EC 1.1.1.41) activity in muscles was not different between PR and R except in masseter muscle from the cheek (+71% in R; P < 0.003), which becomes almost constantly active at weaning for food chewing. Basal and maximally-insulin-stimulated glucose transport rate (GTR) per g tissue wet weight in rectus abdominis muscle were significantly higher in R calves (+31 and 41% respectively; P < 0.05). GLUT4 protein contents did not differ in muscles from PR and R except in masseter (+74% in R; P < 0.05) indicating that the increased GTR in rectus abdominis cannot be accounted for by an enhanced GLUT4 expression. GLUT4 mRNA levels did not differ between the two groups of animals in all muscles suggesting a regulation of GLUT4 at the protein level in masseter. GLUT4 number expressed on a per cell basis was lower in adipose tissue from R calves (-39%; P < 0.05) and higher in internal than in peripheral adipose tissues. In summary, the regulation of GLUT4 in calves at weaning differs markedly from that previously described in rodents (for review, see Girard et al. 1992). Furthermore, significant inter-individual variations were shown for metabolic activities in muscle and for biochemical variables in adipose tissue.

Abdomen↗
PubMed1997

Obesity and GnRH action. Report of a case with contribution by peripherally derived estrogens.

BACKGROUND: Gonadotropin-releasing hormone agonists (GnRH-a) are effective in reducing the pituitary release of gonadotropins, which, in turn, decrease ovarian steroidogenesis. The resulting menopausal state decreases the volume and vascular supply to uterine leiomyomas. Peripheral adipose tissue also contributes significantly to the circulatory estrogen pool, which is formed independent of pituitary function. As such, obesity may interfere with depot leuprolide acetate effects, allowing normal estrogen levels despite gonadotropin suppression. CASE: A premenopausal, morbidly obese woman was referred for treatment of menorrhagia and uterine leiomyomas. Despite administration of depot leuprolide, a GnRH-a, she continued to bleed heavily. Serum estradiol levels remained in the normal range, with suppression of follicle-stimulating hormone (FSH) levels. The desired hypoestrogenic effect from GnRH-a administration was thought to be negated by estradiol levels arising from peripherally derived conversion of adrenal androgens in adipose tissue. A GnRH stimulation test was performed to evaluate the responsiveness of the pituitary to the above therapy. While FSH was suppressed and unresponsive to stimulation, estradiol remained unchanged. CONCLUSION: Peripheral production of estrogen appears to be unaffected by leuprolide administration. Consideration should be given to the patient's body habitus when administering a GnRH suppressant. Morbidly obese patients possess an unlimited reservoir for peripheral estrogen synthesis.

Adipose Tissue↗
PubMed2005

Increased bone adiposity and peroxisomal proliferator-activated receptor-gamma2 expression in type I diabetic mice.

Decreased bone mass, osteoporosis, and increased fracture rates are common skeletal complications in patients with insulin-dependent diabetes mellitus (IDDM; type I diabetes). IDDM develops from little or no insulin production and is marked by elevated blood glucose levels and weight loss. In this study we use a streptozotocin-induced diabetic mouse model to examine the effect of type I diabetes on bone. Histology and microcomputed tomography demonstrate that adult diabetic mice, exhibiting increased plasma glucose and osmolality, have decreased trabecular bone mineral content compared with controls. Bone resorption could not completely account for this effect, because resorption markers (tartrate-resistant acid phosphatase 5b, urinary deoxypyridinoline excretion, and tartrate-resistant acid phosphatase 5 mRNA) are unchanged or reduced at 2 and/or 4 wk after diabetes induction. However, osteocalcin mRNA (a marker of late-stage osteoblast differentiation) and dynamic parameters of bone formation were decreased in diabetic tibias, whereas osteoblast number and runx2 and alkaline phosphatase mRNA levels did not differ. These findings suggest that the final stages of osteoblast maturation and function are suppressed. We also propose a second mechanism contributing to diabetic bone loss: increased marrow adiposity. This is supported by increased expression of adipocyte markers [peroxisome proliferator-activated receptor gamma2, resistin, and adipocyte fatty acid binding protein (alphaP2)] and the appearance of lipid-dense adipocytes in diabetic tibias. In contrast to bone marrow, adipose stores at other sites are depleted in diabetic mice, as indicated by decreased body, liver, and peripheral adipose tissue weights. These findings suggest that IDDM contributes to bone loss through changes in marrow composition resulting in decreased mature osteoblasts and increased adipose accumulation.

Adipose Tissue↗
PubMed1995

Assimilation and mobilization of triglycerides in subcutaneous abdominal and femoral adipose tissue in vivo in men: effects of androgens.

Studies on regional differences of adipose tissue metabolism have mainly been performed in vitro. To allow measurements of lipid uptake in vivo in man, radioactive label from [9,10-3H]oleic acid in 80 g orally administered milk fat was measured after 4 h in abdominal and femoral sc adipose tissues in 28 middle-aged, abdominally obese men. Radioactivity was measured in adipose tissue triglycerides extracted from needle biopsies. Lipoprotein lipase (LPL) activity was also measured. Uptake of label in triglycerides and LPL activity were higher (20% and 15%, respectively; P < 0.05) in the abdominal compared to the femoral adipose tissue region. The men were then randomly assigned to three groups, receiving testosterone (T), dihydrotestosterone, or placebo, for 9 months. After 2 months of treatment, the procedure of administration of label was repeated, this time using [U-14C]oleic acid as a marker. Measurements of radioactive label was then performed after 4 h and monthly up to 7 months. Supplementation with T was followed by an inhibited uptake of label in triglycerides (34%; P < 0.05), lower LPL activity (48%; P < 0.05), and a shorter t1/2 (30%; P < 0.05) in the abdominal adipose tissue region compared with the dihydrotestosterone and placebo groups. No significant effect of T on triglyceride uptake, LPL activity, or t1/2 was found in sc femoral adipose tissue. It was concluded that the turnover rate of depot triglycerides is more rapid in abdominal compared to femoral sc adipose tissue in men. Furthermore, T supplementation inhibits triglyceride uptake and LPL activity and causes a more rapid turnover of triglycerides only in the sc abdominal adipose tissue region. These results demonstrate the marked effects of T on adipose tissue metabolism in vivo and suggest that T is an important regulator of the proportion of depot fat mass in central and peripheral adipose tissue in men.

Abdomen↗
PubMed1996

Adipose tissue extraction of circulating insulin in anaesthetized Zucker obese rats.

OBJECTIVE: To determine whether adipose tissue removes a significant proportion of circulating insulin in the obese rat in vivo. DESIGN: Blood samples were obtained from the carotid artery and the venous side of hind leg muscle, epididymal fat pads and liver (portal and suprahepatic veins), they were used for estimation of insulin disappearance across the tissue. SUBJECTS: Anaesthetized Zucker lean (Fa/?) and obese (fa/fa) adult male rats. MEASUREMENTS: Blood flow, glycaemia and insulinaemia. RESULTS: In lean rats, the liver accounted for practically all insulin extraction (498 +/- 149 fmol.s-1), removing more than half of the portal insulin in a single pass. In the obese rats, the liver extracted a similar amount in absolute terms (397 +/- 108 fmol.s-1), representing only 16% of portal insulin. In the hind leg muscle of both groups and in the adipose tissue of lean rats, insulin balances were not different from zero; but in obese rats, adipose tissue extracted a similar amount of insulin (405 +/- 127 fmol.s-1) to that removed by the liver. CONCLUSIONS: In the Zucker obese rat, peripheral adipose tissue removes as much insulin from the blood as the liver does, in contrast with lean rats, in which the latter is responsible for practically all insulin extraction.

Adipose Tissue↗
PubMed2006

Neuronal pathway from the liver modulates energy expenditure and systemic insulin sensitivity.

Coordinated control of energy metabolism and glucose homeostasis requires communication between organs and tissues. We identified a neuronal pathway that participates in the cross talk between the liver and adipose tissue. By studying a mouse model, we showed that adenovirus-mediated expression of peroxisome proliferator-activated receptor (PPAR)-g2 in the liver induces acute hepatic steatosis while markedly decreasing peripheral adiposity. These changes were accompanied by increased energy expenditure and improved systemic insulin sensitivity. Hepatic vagotomy and selective afferent blockage of the hepatic vagus revealed that the effects on peripheral tissues involve the afferent vagal nerve. Furthermore, an antidiabetic thiazolidinedione, a PPARg agonist, enhanced this pathway. This neuronal pathway from the liver may function to protect against metabolic perturbation induced by excessive energy storage.

Adipose Tissue↗
PubMed1994

Peripheral and abdominal adiposity in childhood obesity.

The aim of this work was to evaluate peripheral and abdominal adipose tissue (AT) content detected by MRI in normal weight and obese children, to compare MRI data with simple anthropometric indexes and to estimate intrabdominal adipose tissue (IAT) influence on cardiovascular risk factors. The subjects were 23 obese and 21 normal weight children aged 10 to 15 years. The following measurements were carried out: MRI analysis at lumbar level with definition of subcutaneous adipose tissue (SAT) area and IAT area; arm fat area (AFA); thigh fat area (TFA) and waist/hip ratio from anthropometry. SAT (353 +/- 94 cm2) was predominant compared with IAT (49 +/- 21 cm2) in obese as well as in controls (SAT: 79 +/- 61 cm2; IAT: 22 +/- 11 cm2). No differences in SAT/IAT ratio were found for sex and puberty, either in obese subjects or in controls. SAT and IAT were significantly related in controls (r = 0.77, P < 0.0001), but not in obese subjects (r = 0.12, P = 0.59). IAT was related to total and LDL cholesterol and triglycerides levels (r = 0.54, P < 0.02, r = 0.60, P < 0.01, r = 0.46, P < 0.04, respectively) in obese children. AFA and TFA from anthropometry significantly underestimated AT compared with MRI in both groups. Methods agreement analysis showed unacceptable results for anthropometry. It was concluded that childhood obesity has a subcutaneous adipose pattern with no differences between the sexes. IAT already begins to have clinical significance since it has a relationship to some cardiovascular risk factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1998

Reduced BAT function as a mechanism for obesity in the hypophagic, neuropeptide Y deficient monosodium glutamate-treated rat.

Neuropeptide Y (NPY) exerts effects on food intake at the level of the paraventricular nucleus (PVN), which receives a dense projection from the arcuate nucleus. Monosodium glutamate (MSG) has been shown to induce hyperadiposity despite hypophagia associated with chemical ablation of the arcuate nucleus. We investigated the mechanism for the excess fat accumulation by studying the time course of changes in brain NPY content, food intake, leptin levels and BAT GLUT4 content after neonatal MSG treatment. Male rat pups were injected with MSG or saline vehicle on days 2, 4, and 6 and examined at 30 and 90 days. Plasma leptin, body mass, length, adipose tissue mass and brown fat GLUT4 were measured and brains dissected for measurement of NPY content. By 30 days, NPY concentrations were reduced in the arcuate nucleus and anterior hypothalamus, and animals tended to be hypophagic. Peripheral adipose tissue levels were less than controls, in line with their low leptin concentrations. At 90 days, MSG treatment was associated with marked reductions in NPY concentrations in several hypothalamic areas, including the PVN and arcuate nucleus, along with increased adiposity and plasma leptin. Animals also displayed marked hypophagia. Levels of GLUT4 transporter were reduced in brown adipose tissue at both ages. The early decrease in brown fat GLUT4 suggests an impairment of the hypothalamic sympathetic input to brown fat which disrupts thermogenesis, contributing to the development of adiposity in the presence of hypophagia.

Adipose Tissue, Brown↗
PubMed2004

Novel associations between bioavailable estradiol and adipokines in elderly women with different phenotypes of obesity: implications for atherogenesis.

BACKGROUND: Peripheral adiposity confers protection against diabetes and atherosclerosis in elderly women. The underlying mechanisms, however, remain to be elucidated. METHODS AND RESULTS: On the basis on dual-energy X-ray absorptiometry measurements of central fat mass (CFM) and peripheral fat mass (PFM), we identified 290 elderly women with distinct forms of body fat distribution (lean, peripheral obesity, central obesity, or general obesity). Study parameters were plasma tumor necrosis factor-alpha, interleukin (IL)-6, adiponectin, estradiol, sex hormone-binding globulin, insulin resistance, and aortic calcification, graded on lateral radiography. In peripherally and generally obese women, plasma estradiol and insulin resistance were significantly lower, whereas sex hormone-binding globulin and adiponectin were significantly higher compared with centrally obese women independent of age, body mass index, total fat mass, and smoking habits (all P<0.05). After adjustment for these confounders, IL-6 in centrally obese women was comparable with that seen in generally obese (similar high CFM%) but significantly higher than in peripherally obese women and lean women (low CFM%). Atherosclerosis was less severe in generally obese (2.5+/-0.3) compared with centrally obese women (5.0+/-0.7, P=0.001). In multiple regression analysis, total fat mass, body fat distribution, insulin resistance, estradiol, current smoking, treated hyperlipidemia, and treated hypertension contributed independently to the variation of aortic calcification (R=0.55, SEE=3.60, P<0.001). CONCLUSIONS: Abundant presence of PFM in generally obese women is associated with increased plasma adiponectin and higher insulin sensitivity, which could explain the apparent protection against the atherogenic effects of IL-6 derived from CFM. Low peripheral exposure to estradiol appears to be a sine qua non of maintained adiponectin secretion from PFM.

Absorptiometry, Photon↗
PubMed1991

Physiology of exercise in the cold.

Recreational and job requirements have increased the incidence in which humans exercise in cold environment. Understanding the physiological responses while exposed to cold entails knowledge of how exercise and cold interact on metabolic, cardiopulmonary, muscle and thermal aspects of human performance. Where possible, distinction are made between responses in cold air and cold water. While there is no consensus for diets most appropriate for working cold exposures, the evidence is strong that adequate amounts of carbohydrate are necessary. Carbohydrate loading appears to be efficacious, as it is for other athletic endeavours. Contrary to conventional wisdom, the combination of exercise and cold exposure does not act synergistically to enhance metabolism of fats. Free fatty acid (FFA) levels are not higher, and may be lower, with exercise in cold air or water when compared to corresponding warmer conditions. Glycerol, a good indicator of lipid mobilisation, is likewise reduced in the cold, suggesting impaired mobilisation from adipose tissue. Catecholamines, which promote lipolysis, are higher during exercise in cold air and water, indicating that the reduced lipid metabolism is not due to a lack of adequate hormonal stimulation. It is proposed that cold-induced vasoconstriction of peripheral adipose tissue may account, in part, for the decrease in lipid mobilisation. The respiratory exchange ratio (RER) is often similar for exercise conducted in warm and cold climates, suggesting FFA utilisation is equivalent between warm and cold exposures. The fractional portion of oxygen consumption (VO2) used for FFA combustion may decrease slightly during exercise in the cold. This decrease may be related to a relative decrease in oxygen delivery (i.e. muscle blood flow) or to impaired lipid mobilisation. Venous glucose is not substantially altered during exercise in the cold, but lactate levels are generally higher than with work in milder conditions. The time lag between production of lactate within the muscle and its release into the venous circulation may be increased by cold exposure. Minute ventilation is substantially increased upon initial exposure to cold, and a relative hyperventilation may persist throughout exercise. With prolonged exercise, though, ventilation may return to values comparable to exercise in warmer conditions. Exercise VO2 is generally higher in the cold, but the difference between warm and cold environments becomes less as workload increases. Increases in oxygen uptake may be due to persistence of shivering during exercise, to an increase in muscle tonus in the absence of overshivering, or to nonshivering thermogenesis. Heart rate is often, but not always, lower during exercise in the cold.(ABSTRACT TRUNCATED AT 400 WORDS)

Body Temperature Regulation↗
PubMed2002

Chronic ethanol consumption increases plasma leptin levels and alters leptin receptors in the hypothalamus and the perigonadal fat of C57BL/6 mice.

BACKGROUND: Leptin, a protein secreted from adipocytes, and leptin receptors, expressed in the hypothalamus and fat tissue, regulate energy balance and adiposity. Leptin receptors exist as several forms that are delineated by the length of their cytoplasmic domains. Only the longest form is physiologically active through stimulation of the signal transducers and activators of transcription (STAT) second messenger system. Previous studies demonstrated that chronic ethanol consumption increases body adiposity and circulating leptin levels. This study examined the effect of chronic alcohol intake on the expression of leptin receptors and associated STAT second messengers in the hypothalamus and fat tissue. METHODS: Female C57BL/6 mice were given water or 20% w/v ethanol and Purina 5001 laboratory chow ad libitum for 2 or 5 weeks. Plasma leptin levels were determined by radioimmunoassay and body adiposity was evaluated by measuring the amount of perigonadal fat. Expression of leptin receptors as well as STAT molecules in whole-cell lysates of the hypothalamus and the perigonadal fat were assayed by Western blot analysis. RESULTS: Plasma leptin and perigonadal fat were increased after 5 weeks. The overall expression of leptin receptors was increased while the expression of the physiologically active long form of leptin receptor was decreased in the hypothalamus and the perigonadal fat of ethanol-consuming mice. Ethanol consumption also decreased hypothalamic expression of STAT3, a protein associated with leptin receptor activation in this region of the brain. In contrast, STAT1, a protein associated with leptin receptor activation in adipose tissue, was significantly elevated in the perigonadal fat of ethanol-consuming mice. CONCLUSIONS: Chronic ethanol consumption increases the circulating level of leptin, and this is accompanied by altered expression of leptin-sensing molecules in the hypothalamus and peripheral adipose tissue. These results suggest that chronic ethanol intake affects metabolism by altering the leptin system that regulates energy balance.

Adipose Tissue↗
PubMed1976

Effects of hypophysectomy and acute growth hormone treatment upon glucose metabolism in adipose tissues and isolated adipocytes of rats.

Glucose oxidation and incorporation into lipid were measured in epididymal adipose tissues and isolated adipose cells of normal and hypophysectomized rats in an effort to determine whether the acute hypoglycemic effect of a systemic growth hormone (GH) injection was related to alterations in the glucose metabolism of adipose tissue. The rats were fed rat chow or a high sucrose diet and received 100 mug GH intraperitoneally 30 minutes or three and one-half hours before sacrifice. Hypophysectomized rats showed a lower plasma glucose as compared with normal rats on both diets. Thirty minutes after a GH injection there was a further decrease of the plasma glucose which, however, was not present in those rats receiving GH three and one-half hours before sacrifice. Adipose tissues from hypophysectomized rats fed the high sucrose diet showed a blunted insulin sensitivity as compared with normal rats on a similar diet. The insulin sensitivity of these tissues was further decreased 30 minutes after a GH injection. Basal glucose metabolism of isolated adipocytes from hypophysectomized rats, as compared with normal rats, was depressed if they were fed rat chow, was at normal levels if they were fed the high sucrose diet and was increased if they were fed the sucrose diet and received triiodothyronine and cortisone supplements. No manipulations of diet or hormonal treatments made the isolated adipocyte from hypophysectomized rats sensitive to insulin either 30 minutes or three and one-half hours after a GH injection. Since basal glucose utilization is not enhanced by GH injection and both the blunted insulin sensitivity of adipose tissue and the absent insulin sensitivity of adipopocytes would be expected to produce hyperglycemia rather than hypoglycemia, it is concluded that immediate systemic effects of a GH injection on carbohydrate metabolism are not related to changes in glucose metabolism of the peripheral adipose tissues.

Adipose Tissue↗
PubMedDate not supplied

Diabetes: insulin resistance and derangements in lipid metabolism. Cure through intervention in fat transport and storage.

We present multiple findings on derangements in lipid metabolism in type 2 diabetes. The increase in the intracellular deposition of triglycerides (TG) in muscles, liver and pancreas in subjects prone to diabetes is well documented and demonstrated to attenuate glucose metabolism by interfering with insulin signaling and insulin secretion. The obesity often associated with type 2 diabetes is mainly central, resulting in the overload of abdominal adipocytes with TG and reducing fat depot capacity to protect other tissues from utilizing a large proportion of dietary fat. In contrast to subcutaneous adipocytes, the central adipocytes exhibit a high rate of basal lipolysis and are highly sensitive to fat mobilizing hormones, but respond poorly to lipolysis restraining insulin. The enlarged visceral adipocytes are flooding the portal circulation with free fatty acids (FFA) at metabolically inappropriate time, when FFA should be oxidized, thus exposing nonadipose tissues to fat excess. This leads to ectopic TG accumulation in muscles, liver and pancreatic beta-cells, resulting in insulin resistance and beta-cell dysfunction. This situation, based on a large number of observations in humans and experimental animals, confirms that peripheral adipose tissue is closely regulated, performing a vital role of buffering fluxes of FFA in the circulation. The central adipose tissues tend to upset this balance by releasing large amounts of FFA. To reduce the excessive fat outflow from the abdominal depots and prevent the ectopic fat deposition it is important to decrease the volume of central fat stores or increase the peripheral fat stores. One possibility is to downregulate the activity of lipoprotein lipase, which is overexpressed in abdominal relatively to subcutaneous fat stores. This can be achieved by gastrointestinal bypass or gastroplasty, which decrease dietary fat absorption, or by direct means that include surgical removal of mesenteric fat. Indirect treatment consists of the compliant application of drastic lifestyle change comprising both diet and exercise and pharmacotherapy that reduces mesenteric fat mass and activity. The first step should be an attempt to effectively induce a lifestyle change. Next comes pharmacotherapy including acarbose, metformin, PPARgamma, or PPARgammaalpha agonists, statins and orlistat, estrogens in postmenopausal women or testosterone in men. Among surgical procedures, gastric bypass has been proven to produce beneficial results in advance of other surgical techniques, the evidence basis of which still needs strengthening.

Animals↗
PubMed2001

Altered renal sodium handling in men with abdominal adiposity: a link to hypertension.

OBJECTIVES: Central adiposity, insulin resistance and hypertension are clearly interrelated but the mechanisms underlying this association have not been thoroughly elucidated. As renal sodium handling plays a central role in salt-sensitive forms of hypertension, we investigated the relation of renal tubular sodium handling to abdominal adiposity, blood pressure and insulin sensitivity. DESIGN: Population-based study. PARTICIPANTS: Five hundred and fifty-five untreated Olivetti male workers, aged 25-75 years. SETTING: Olivetti factory medical centers in Pozzuoli and Marcianise (Naples, Italy) MAIN OUTCOME MEASURES: Anthropometric indices, serum insulin, homeostatic model assessment index of insulin sensitivity, blood pressure, fractional excretions of uric acid and exogenous lithium (as markers of renal tubular sodium handling). RESULTS: In univariate analysis, measures of central adiposity (i.e. sagittal abdominal diameter and umbilical circumference) were directly correlated with serum insulin (P < 0.001) and blood pressure levels (P < 0.001) and inversely associated with the fractional excretions of uric acid and lithium (P = 0.01-0.001). In multiple linear regression analysis, the same anthropometric indices but not the measures of peripheral adiposity (arm circumference and tricipital skinfold thickness), were significant predictors of the fractional excretion of uric acid and lithium, independently of age, blood pressure and serum insulin levels (P = 0.01-0.001). CONCLUSIONS: Abdominal adiposity was associated with altered renal tubular sodium handling apart from insulin resistance and high blood pressure. The data indicate that men with prevalent abdominal adiposity have an enhanced rate of tubular sodium reabsorption, mainly at proximal sites. These findings provide a possible mechanistic link between central adiposity and salt-dependent hypertension.

Abdomen↗
PubMed1988

The potency of fluorinated ether anesthetics correlates with their 19F spin-spin relaxation times in brain tissue.

In this study, four fluorinated ether anesthetics and one non-anesthetic fluorinated alkane were observed in rat brain and adipose tissue using 19F-NMR spectroscopy. Measurements of 19F spin-spin relaxation times (T2) of the anesthetics in brain revealed T2 values (0.5-4.5 msec) that correlated linearly with the anesthetic potency (ED50) of the drugs. The non-anesthetic was present at very low concentrations in brain and had a T2 value (18.5 msec) far longer than that of any of the anesthetics. All of the drugs were present at high concentration in peripheral adipose tissue. 19F T2 values for these drugs in adipose tissue (200-400 msec) were far larger than the values observed in brain and did not correlate with anesthetic potency. These results indicate that volatile anesthetic molecules have a specific affinity for neural tissue and that immobilization of anesthetic molecules in brain correlates with anesthetic potency. The results with adipose tissue suggest that the interaction of anesthetic with brain tissue cannot be explained by a simple partition of these drugs into lipid.

Adipose Tissue↗
PubMed2000

[Leptin levels in peripheral blood and bone marrow in orthopedic patients].

Leptin is a protein with hormonal activity and is produced mainly by adipocytes. Its primary function in the human organism is regulation of the calorie intake via the anorectic action in the hypothalamus. Leptin participates also in the regulation of haematopoiesis and immunity processes. There are many data on leptin production by peripheral adipose tissue and it is also known that leptin is produced by adipocytes of bone marrow. It was assumed for a long time that adipocytes of bone marrow are not only a passive source of energy but have, similarly as stromal cells, a regulatory function. However, it is not clear in what way the adipose tissue of bone marrow participates in the regulation of haematopoiesis and what role is played in this relationship by leptin production. The authors attempted to assemble in their small study data on leptin production in bone marrow and at the same time parameters of lipids of bone marrow which can be assessed by cytological examination. The authors examined 16 patients (9 men and 7 women) subjected to orthopaedic surgery. They assessed leptin concentrations in sera obtained from peripheral blood and bone marrow, and at the same time they assessed by morphological examination in smears of bone marrow some parameters associated with lipids. The authors found that serum leptin levels from bone marrow are significantly lower than in peripheral blood (p < 0.0005). These values correlate closely (r = +0.77, p < 0.0005). The authors found also a positive correlation between serum leptin (r = +0.56, p < 0.02) and bone marrow leptin (r = +0.72, p < 0.002) and the body mass index (BMI). A positive correlation was found also between serum (r = +0.65, p < 0.006) and bone marrow leptin (r = +0.80, p < 0.0002) and age. The authors did not detect any significant correlations between parameters of the lipids of bone marrow and leptin levels in serum and bone marrow. The assembled results can in combination with data from the literature indicate that the actual amount of leptin in bone marrow is influenced rather by its consumption by haematopoietic tissue than by its production.

Adolescent↗
PubMed2005

Lipodystrophy associated with highly active anti-retroviral therapy for HIV infection: the adipocyte as a target of anti-retroviral-induced mitochondrial toxicity.

The lipodystrophy syndrome and associated metabolic alterations are the most prevalent adverse effects in HIV-infected patients taking highly active anti-retroviral therapy (HAART). This syndrome involves profound disturbances in adipose tissue. The toxic effect of nucleoside reverse transcriptase inhibitors on mitochondrial function is a major contributor to the lipodystrophy syndrome. Although adipocytes were not expected to be preferential targets of mitochondrial toxicity, recent re-evaluation of the role of mitochondria in white adipocytes helps to explain the molecular basis of HAART-associated lipodystrophy. Adipocytes are a source of paracrine and endocrine signals that influence adipocyte biology and systemic metabolism. Mitochondrial disturbances elicited by HAART result in an abnormal perception of the bioenergetic status by adipocytes, thus leading to enhancement of catalytic pathways and apoptosis in peripheral adipose tissue, alterations in the differentiation of brown versus white adipocytes, and the release of hormonal signals that lead to systemic metabolic disturbances.

Adipocytes↗