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PubMed1998

Association of fasting insulin with serum lipids and blood pressure in Kuwaiti children.

To examine the association of hyperinsulinemia with the atherogenic risk profile in children, we studied the relationships of the fasting plasma insulin level with indices of obesity (body mass index [BMI] and sum of triceps and subscapular skinfold thickness [SFT]), body fat distribution (waist to hip ratio [WHR]), serum lipid, lipoprotein, and apolipoprotein levels, and blood pressure in a case-control study of 460 Kuwaiti prepubertal obese children aged 6 to 13 years matched by age and sex to 460 prepubertal non-obese controls. Obese children were ascertained in a representative cross-sectional study of 2,400 school children. Fasting insulin levels were positively correlated (P < .001) with serum triglyceride (TG) and very-low-density lipoprotein (VLDL) cholesterol levels and negatively correlated with high-density lipoprotein (HDL) cholesterol levels. No significant associations were observed between insulin and total cholesterol (TC), cholesterol, low-density lipoprotein (LDL) or apolipoprotein A-I (apo A-I). Stronger associations of insulin levels with lipoprotein fractions were observed in obese versus non-obese controls. Obese children had a higher concentration of apo B and a lower apo A-I:B ratio (P < .001). Insulin and the insulin to glucose ratio increased with age in obese children, whereas there were slight changes in non-obese children. TG and HDL cholesterol levels and systolic blood pressure (SBP) were significantly different across insulin quartiles in boys and girls. We conclude that the fasting plasma insulin level may be used as a marker for the development of obesity-associated metabolic disorders and elevated blood pressure in children.

Adipose Tissue↗
PubMed2003

Endothelial markers and HIV infection in the era of highly active antiretroviral treatment.

Many circumstances can induce activation and/or injury of the endothelium that plays a role in the development of vascular complications. Raised plasma levels of endothelial markers such as von Willebrand factor (vWF), soluble thrombomodulin (sTM) and soluble vascular cell adhesion molecule-1 (sVCAM-1) have a prognostic and/or diagnostic value. Human immunodeficiency virus-infected patients (HIV+) have a clustering of conditions that activate or injure the endothelium. Highly active antiretroviral treatment produces adverse effects such as dyslipemia, insulin resistance (IR) and body fat changes (named lipodystrophy syndrome) which may contribute to aggravate their endothelial perturbation. The aim of this study was to measure lipid profile, insulin resistance status, and endothelial markers in 38 HIV+ naive of antiretroviral treatment and 63 HIV+ under highly active antiretroviral treatment (33 with lipodystrophy syndrome and 30 without it). Body fat distribution was also evaluated by dual-energy X-ray absorptiometry (DEXA) analysis. Thirty-one HIV negative subjects were used as controls. We looked for association between variables. Insulin resistance status was a common finding in the four groups. Lipodystrophic patients presented an atherothrombotic lipid profile [elevated levels of triglycerides (TG), low-density lipoprotein cholesterol (LDL-chol) and apolipoprotein-B (APO-B)] and a strong loss of fat in legs and arms (lipoatrophy). All endothelial markers evaluated in our naive patients were higher as compared to control group. sVCAM-1 in HIV+ under therapy without lipodystrophy syndrome showed significantly decreased levels as compared to naive group (487 vs. 666 ng/ml) and vWF and sTM tended to diminish although they did not show a significant difference (130% vs. 170%, 41 vs. 45 ng/ml, respectively). Lipodystrophic patients showed a tendency to increased levels of endothelial activation markers (sVCAM-1: 500 ng/ml and vWF: 154%) together with significantly increased levels of an endothelial injury marker (sTM: 50 ng/ml) with respect to HIV+ under therapy without lipodystrophy syndrome. Plasma levels of sTM, as an endothelial injury marker, correlated with peripheral lipoatrophy (rho = -0.357) in lipodystrophic patients. In conclusion, despite the beneficial immunology effect of highly active antiretroviral treatment and the apparent decrease in the endothelial perturbation, the patients who develop lipodystrophy present altered endothelial markers and other risk factors, such as IR and dyslipemia, which turn them into a high atherothrombotic risk group.

Absorptiometry, Photon↗
PubMedDate not supplied

Insulin resistance: current concepts.

Insulin sensitivity varies greatly within the general population; factors contributing to this variability include genetic pre-disposition, obesity, unfavorable body fat distribution, and lack of physical activity. Impaired insulin sensitivity may lead to impaired glucose tolerance and, even in individuals with modest insulin deficiency, to the development of type 2 diabetes mellitus. Of equal concern in patients with impaired insulin sensitivity is the development of the insulin resistance syndrome, in which hypertension, dyslipidemia, and impaired glucose tolerance form a cluster of risk factors for cardiovascular disease. Treatment of insulin resistance includes metformin and the thiazolidinedione troglitazone. Both drugs have been shown to be effective in the treatment of insulin resistance, one of the central abnormalities in type 2 diabetes mellitus. The purpose of this study was to review the current understanding of insulin resistance and its implications for the treatment of type 2 diabetes mellitus. To do this, a MEDLINE search of the clinical literature was conducted and the content analyzed.

Diabetes Mellitus, Type 2↗
PubMed2000

Adipose tissue as an endocrine organ.

The discovery of leptin in the mid-1990s has focused attention on the role of proteins secreted by adipose tissue. Leptin has profound effects on appetite and energy balance, and is also involved in the regulation of neuroendocrine and immune function. Sex steroid and glucocorticoid metabolism in adipose tissue has been implicated as a determinant of body fat distribution and cardiovascular risk. Other adipose products, for example, proinflammatory cytokines, complement factors and components of the coagulation/fibrinolytic cascade, may mediate the metabolic and cardiovascular complications associated with obesity.

Adipose Tissue↗
PubMed1998

Visceral obesity and the risk of ischaemic heart disease: insights from the Québec Cardiovascular Study.

There is no doubt that visceral obesity increases the susceptibility to IHD, emphasizing the need to consider this condition in the risk management of IHD. The use of CT or MRI as clinical tools to assess visceral adipose tissue accumulation does not appear to be justified, however, mostly because of the costs of the procedures and the limited availability of the necessary apparatus. The waist:hip ratio has been used extensively as an indicator of body fat distribution. However, it has been shown that the waist:hip ratio is less accurate than the waist circumference alone or the sagittal diameter in predicting visceral adipose tissue accumulation, particularly when monitoring changes in visceral adipose tissue mass over time.79 Also, the prediction of visceral adipose tissue levels by the waist circumference alone, as opposed to the waist:hip ratio, does not appear to be affected by gender or by the degree of obesity.80 For these reasons we have proposed that the waist circumference should be systematically measured in managing the risk of IHD. It is a simple and inexpensive measurement to perform, while providing potentially critical information on the risk profile of both men and women.80 We believe that identification of viscerally obese patients, a high-risk population for IHD, should be considered as a critical step in the risk management of IHD.

Cholesterol, LDL↗
PubMed1998

Clinical implications of the insulin resistance syndrome.

Insulin resistance syndrome (IRS), also termed syndrome X, is a distinctive constellation of risk factors for the development of type 2 diabetes mellitus and cardiovascular disease. The syndrome's hallmarks are glucose intolerance, hyperinsulinemia, a characteristic dyslipidemia (high triglycerides; low high-density lipoprotein cholesterol, and small, dense low-density lipoprotein cholesterol), obesity, upper-body fat distribution, hypertension, and increased prothrombotic and antifibrinolytic factors. Insulin resistance, caused by a complex of genetic and environmental influences, is now recognized not just as a mechanism contributing to hyperglycemia in type 2 diabetes, but also as an early metabolic abnormality that precedes the development of overt diabetes. The clinical definition of insulin resistance is the impaired ability of insulin (either endogenous or exogenous) to lower blood glucose. In some insulin-resistant individuals, insulin secretion will begin to deteriorate under chronic stress (glucose toxicity) and overt diabetes will result. If not, individuals will remain hyperinsulinemic, with perhaps some degree of glucose intolerance, together with other hallmarks of the IRS. The statistical correlation between hypertension and impaired glucose tolerance is clear, although the mechanism is not yet fully understood. Epidemiologic evidence of insulin resistance as an independent risk factor for atherosclerosis and coronary heart disease (CHD) completed the evolving concept of IRS as the common soil for the development of both diabetes and CHD. No single laboratory test exists for diagnosis of IRS. Rather, IRS remains a clinically evident syndrome that can be suspected on the basis of physical and laboratory findings. This identifies individual patients whom the clinician should screen for associated comorbid conditions, aggressively control cardiovascular risk factors, and tailor drug therapy for optimal benefit. This article provides practical guidelines to achieve these goals and specific strategies to ameliorate cardiovascular and metabolic risk in the IRS.

Albuminuria↗
PubMed2005

Effects of megestrol acetate on pituitary function and end-organ hormone secretion: a post hoc analysis of serum samples from a 12-week study in healthy older men.

BACKGROUND: Megestrol acetate (MA) is a synthetic progestin commonly used to promote weight gain in malnourished older individuals. In small studies, MA administration has been associated with reduced serum cortisol concentrations in patients with cancer or AIDS. The impact of MA on the pituitary secretion of adrenocorticotropic hormone (ACTH) and other hormones is unclear, and the prevalence and extent of hypocortisolemia in older individuals after MA treatment is unknown. A randomized, placebo-controlled study of the effects of testosterone (T) and resistance training (RT) on body composition after MA administration in older men has been reported previously. OBJECTIVE: The purpose of this post hoc analysis was to examine the effect of 12 weeks of MA on pituitary function and end-organ hormone secretion in healthy older individuals using frozen serum samples from that study. METHODS: The previous study was conducted at the Department of Geriatrics, Donald W. Reynolds Center on Aging and the General Clinical Research Center at The University of Arkansas for Medical Sciences, Little Rock, Arkansas. Healthy male volunteers aged 60 to 85 years were recruited from the center and were randomly assigned to 1 of 4 study groups: RT + T, T, RT + placebo (P), or P. Subjects enrolled in the RT groups underwent supervised upper- and lower-body strength-training exercises 3 d/wk at 80% of 1 repetition maximum. Subjects in the groups to receive T received injections of testosterone enanthate 100 mg i.m. QW for 12 weeks. Subjects receiving P were given 1-mL saline injections i.m. QW for 12 weeks. All subjects received MA 800 mg p.o. QD concurrently for 12 weeks. For the present analysis, serum concentrations of the pituitary hormones follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), ACTH, prolactin (PRL), and luteinizing hormone (LH), as well as the end-organ hormones estradiol (E2), cortisol, free T4, and T, were measured in samples obtained at baseline (week 0) and after 12 weeks of MA treatment. RESULTS: Serum samples from 21 men (mean [SD]age, 67.0 [7.3]years; mean [SD] body mass index, 23.1 [10.4] kg/m2; mean [SD] percentage of body fat, 22.5% [8.8%]; RT + T, T, RT + P, and P groups, n = 4, 5, 6, and 6 subjects, respectively) were available from the original study. The mean percentage changes from baseline in serum pituitary hormone concentrations after 12 weeks of MA administration were as follows: TSH, -14.7%; ACTH, -89.5%; PRL, 162.2%; and LH, -49.0%; (P = 0.03, <0.001, <0.001, and <0.001, respectively). The mean (SD) percentage changes from baseline in serum end-organ hormone concentrations with MA at 12 weeks were as follows: E2, 181.6%; and cortisol, -90.8% (both, P < 0.001). In the P and RT + P groups, the mean percentage changes from baseline in T were -84% and -85%, respectively (both, P < 0.001). FSH and free T4 concentrations were not significantly changed. CONCLUSIONS: This analysis of serum samples from healthy older men suggests that MA administration significantly affected the secretion of several pituitary hormones and end-organ hormone synthesis. Most notably, ACTH secretion and serum cortisol levels were statistically significantly suppressed in 20 of 21 subjects, without the development of clinically significant adrenal suppression.

Aged↗
PubMed2003

Genomic approaches to understanding obstructive sleep apnea.

Obstructive sleep apnea (OSA) is an increasingly recognized, common chronic disease in the developed nations and is a complex disease that has high social and economic costs. OSA and its associated 'intermediate' phenotypes-craniofacial structure, body fat distribution and metabolism, and neurological control of the upper airway muscles and of sleep and circadian rhythm-are under a substantial degree of genetic control. Investigating the genetic aetiology of OSA offers a means of better understanding its pathogenesis, with the goal of improving preventive strategies, diagnostic tools and therapies. Molecular studies of OSA itself are in their infancy, but considerable effort and expense has already been expended in attempts to detect genetic loci contributing to OSA-associated intermediate phenotypes, such as obesity. However, many of the fundamental questions relating to the genetic epidemiology of OSA and associated factors remain unanswered. This chapter reviews the current state of knowledge of the genetics of OSA, with a focus on genomic approaches to understanding sleep disorders.

Animals↗
PubMed2006

Energetics reveals physiologically distinct castes in a eusocial mammal.

Eusociality, which occurs among mammals only in two species of African mole-rat, is characterized by division of labour between morphologically distinct 'castes'. In Damaraland mole-rats (Cryptomys damarensis), colony labour is divided between 'infrequent worker' and 'frequent worker' castes. Frequent workers are active year-round and together perform more than 95% of the total work of the colony, whereas infrequent workers typically perform less than 5% of the total work. Anecdotal evidence suggests that infrequent workers may act as dispersers, with dispersal being limited to comparatively rare periods when the soil is softened by moisture. Here we show that infrequent workers and queens increase their daily energy expenditure after rainfall whereas frequent workers do not. Infrequent workers are also fatter than frequent workers. We suggest that infrequent workers constitute a physiologically distinct dispersing caste, the members of which, instead of contributing to the work of the colony and helping the queen to reproduce, build up their own body reserves in preparation for dispersal and reproduction when environmental conditions are suitable.

Animals↗
PubMed2001

Identification of the gene altered in Berardinelli-Seip congenital lipodystrophy on chromosome 11q13.

Congenital generalized lipodystrophy, or Berardinelli-Seip syndrome (BSCL), is a rare autosomal recessive disease characterized by a near-absence of adipose tissue from birth or early infancy and severe insulin resistance. Other clinical and biological features include acanthosis nigricans, hyperandrogenism, muscular hypertrophy, hepatomegaly, altered glucose tolerance or diabetes mellitus, and hypertriglyceridemia. A locus (BSCL1) has been mapped to 9q34 with evidence of heterogeneity. Here, we report a genome screen of nine BSCL families from two geographical clusters (in Lebanon and Norway). We identified a new disease locus, designated BSCL2, within the 2.5-Mb interval flanked by markers D11S4076 and D11S480 on chromosome 11q13. Analysis of 20 additional families of various ethnic origins led to the identification of 11 families in which the disease cosegregates with the 11q13 locus; the remaining families provide confirmation of linkage to 9q34. Sequence analysis of genes located in the 11q13 interval disclosed mutations in a gene homologous to the murine guanine nucleotide-binding protein (G protein), gamma3-linked gene (Gng3lg) in all BSCL2-linked families. BSCL2 is most highly expressed in brain and testis and encodes a protein (which we have called seipin) of unknown function. Most of the variants are null mutations and probably result in a severe disruption of the protein. These findings are of general importance for understanding the molecular mechanisms underlying regulation of body fat distribution and insulin resistance.

Acanthosis Nigricans↗
PubMed2004

Natriuretic peptide clearance receptor alleles and susceptibility to abdominal adiposity.

OBJECTIVE: To test the association of the C(-55)A polymorphism of the natriuretic peptide clearance receptor (NPRC) with blood pressure (BP), overweight/obesity, and body fat distribution in a large male adult population. RESEARCH METHODS AND PROCEDURES: The study population was from a cross-sectional and follow-up study of 787 untreated male participants in the 1994 to 1995 follow-up examination of the Olivetti Heart Study in Naples (356 of whom were examined previously in 1975). BP and anthropometric measures were taken, and biochemical assays were performed. The NPRC gene polymorphism C(-55)A was evaluated by polymerase chain reaction and HgaI digestion. RESULTS: In the whole study population, there was no difference in BP, BMI, and biochemical tests among genotypes. Considering an A(-55) recessive model of inheritance, the AA subjects had lower BMI and waist circumference and lower prevalence of overweight, obesity, and abdominal adiposity as compared with the CC+CA subjects. On reviewing the characteristics of the subgroup previously examined in 1975, the AA subjects had already lower BMI, and their 20-year rate of overweight and obesity was lower than the CC+CA subjects; no difference was observed in the rate of hypertension. DISCUSSION: Male subjects carrying the A(-55)A NPRC genotype had a significantly lower prevalence of overweight, obesity, and abdominal adiposity. They also had a lower 20-year rate of overweight compared with CC+CA individuals. These findings from a large unselected and untreated male population are in keeping with the recent evidence of a powerful lipolytic and lipomobilizing activity of natriuretic peptides.

Abdomen↗
PubMed2006

Weekly changes in basal metabolic rate with eight weeks of overfeeding.

OBJECTIVE: The contribution of basal metabolic rate (BMR) to weight gain susceptibility has long been debated. We wanted to examine whether BMR changes in a linear fashion with overfeeding. Our hypothesis was that BMR does not increase linearly with 1000-kcal/d overfeeding in lean healthy subjects over 8 weeks. The null hypothesis states that BMR increases linearly with 1000-kcal/d overfeeding in lean healthy subjects. RESEARCH METHODS AND PROCEDURES: Initially, 16 lean healthy sedentary subjects completed 2 weeks of weight maintenance feeding at the General Clinical Research Center. The subjects were then overfed by 1000 kcal/d over 8 weeks. BMR was measured under standard conditions each week using indirect calorimetry. RESULTS: Baseline BMR was 1693 +/- 154.5 kcal/d. BMR increased from 1711 +/- 201.3 kcal/d at week 1 of overfeeding to 1781 +/- 171.65 kcal/d at the second week of overfeeding (p = 0.05). BMR fell during the third week of overfeeding to 1729 +/- 179.5 kcal/d (p = 0.05). After 5 weeks of overfeeding, BMR reached a plateau. Thereafter, there was no further change. Comparison of BMR with weeks of overfeeding was significantly different compared with the linear model (p < 0.05). DISCUSSION: Increases in BMR in lean sedentary healthy subjects with 1000-kcal/d overfeeding are not linear over 8 weeks. There seems to be a short-term increase in BMR in the first 2 weeks of overfeeding that is not representative of longer-term changes.

Adiposity↗
PubMed2006

Waist circumference correlates with metabolic syndrome indicators better than percentage fat.

OBJECTIVE: Percent fat is often considered the reference for establishing the magnitude of adipose tissue accumulation and the risk of excess adiposity. However, the increasing recognition of a strong link between central adiposity and metabolic disturbances led us to test whether waist circumference (WC) is more highly correlated with metabolic syndrome components than percent fat and other related anthropometric measures such as BMI. RESEARCH METHODS AND PROCEDURES: BMI, WC, and percent fat, measured by DXA, were evaluated in 1010 healthy white and African-American men and women [age, 48.3 +/- 17.2 (standard deviation) years; BMI, 27.0 +/- 5.3 kg/m(2)]. The associations of BMI, WC, and percent fat with age and laboratory-adjusted health risk indicators (i.e., serum glucose, insulin, triglycerides, high-density lipoprotein cholesterol, blood pressure) in each sex and ethnicity group were examined. RESULTS: For 18 of 24 comparisons, the age- and laboratory-adjusted correlations were lowest for percent fat and in 16 of 24 comparisons were highest for WC. Fifteen of the between-method differences reached statistical significance. With health risk indicator as the dependent variable and anthropometric measures as the independent variable, the contribution of percent fat to the WC regression model was not statistically significant; in contrast, adding WC to the percent fat regression model did make a significant independent contribution for most health risk indicators. DISCUSSION: WC had the strongest associations with health risk indicators, followed by BMI. Although percent fat is a useful measure of overall adiposity, health risks are best represented by the simply measured WC.

Adiposity↗
PubMed2025

Heterogeneous effects of genetic variants and traits associated with fasting insulin on cardiometabolic outcomes.

Elevated fasting insulin levels (FI), indicative of altered insulin secretion and sensitivity, may precede type 2 diabetes (T2D) and cardiovascular disease onset. In this study, we group FI-associated genetic variants based on their genetic and phenotypic similarities and identify seven clusters with distinct mechanisms contributing to elevated FI levels. Clusters fall into two types: "non-diabetogenic hyperinsulinemia," where clusters are not associated with increased T2D risk, and "diabetogenic hyperinsulinemia," where T2D associations are driven by body fat distribution, liver function, circulating lipids, or inflammation. In over 1.1 million multi-ancestry individuals, we demonstrated that diabetogenic hyperinsulinemia cluster-specific polygenic scores exhibit varying risks for cardiovascular conditions, including coronary artery disease, myocardial infarction (MI), and stroke. Notably, the visceral adiposity cluster shows sex-specific effects for MI risk in males without T2D. This study underscores processes that decouple elevated FI levels from T2D and cardiovascular risk, offering new avenues for investigating process-specific pathways of disease.

Humans↗
PubMed1999

Serum glucagon concentration and hyperinsulinaemia influence renal haemodynamics and urinary protein loss in normotensive patients with central obesity.

OBJECTIVES: Insulin-resistance syndrome and hyperinsulinaemia are linked with cardiovascular disease (CVD) in the obese population. In particular, cardiovascular risk is more frequent in central obesity and is associated with microalbuminuria (MA). MA and changes of glomerular permeability to proteins in obesity might be related with renal haemodynamic modifications (that is glomerular hyperfiltration). Since glucagon is physiologically involved in renal haemodynamic regulation, the purpose of this study was to examine whether changes of circulating glucagon levels might haemodynamically induce MA and proteinuria in patients with central obesity. SUBJECTS: Forty normotensive obese out-patients, 22 with central (CO group) and 18 with peripheral (PO group) body fat distribution and 11 healthy subjects. MEASUREMENTS: Serum insulin and glucagon concentrations (fasting and after oral glucose tolerance test (OGTT)) by radio immuno assay (RIA); glomerular filtration rate (GFR, isotopic); total clearances and urinary excretion rates of albumin (AER), IgG (IgGER) and alpha1 microglobulin (computerized immunonephelometry). RESULTS: GFR and insulin concentrations (fasting and during OGTT) were higher in the CO than the PO group. Fasting glucagon concentrations were increased, and not physiologically suppressed during OGTT in patients with CO (fasting, P<0.05; OGTT 60 and 120 min, P<0.001 vs PO group). Moreover, glucagon concentrations were significantly correlated with GFR in the CO group (fasting, r=0.49, P<0.05; 60 min after OGTT, r=0.58, P<0.01); whereas no correlations were found in the PO group. Higher AER (P<0.001), IgGER (P<0.001) and alpha1 microglobulin (P<0.05) urinary concentrations were found in patients with CO than in the PO group. CONCLUSIONS: The increase of serum glucagon concentrations may be associated with the enhancement of GFR in patients with central obesity. Glomerular hyperfiltration might influence the development of MA and of proteinuria by means of a haemodynamic mechanism so contributing to increase the risk of renal microvascular complications and of CVD in central obesity.

Adult↗
PubMed2001

Adipose depot-specific expression of cIAP2 in human preadipocytes and modulation of expression by serum factors and TNFalpha.

BACKGROUND: Visceral obesity is more closely associated with many deleterious metabolic sequelae than obesity per se. The identification of properties that distinguish fat cells of the omentum from adipocytes situated elsewhere in the body may lead to the development of therapeutic strategies targeting visceral obesity. We have previously demonstrated that cIAP2 mRNA is significantly overexpressed in omental (Om) compared with subcutaneous (Sc) adipocytes. This molecule is involved in the TNFalpha signalling pathway and may inhibit apoptosis. OBJECTIVE: To examine the effect of serum agents and TNFalpha upon cIAP2 mRNA expression in human primary culture preadipocytes. DESIGN: Paired omental and subcutaneous adipose tissue biopsies were obtained from 11 patients, nine female and two male, with ages ranging from 29 to 82. These were cultured in either serum containing medium or serum-free medium with or without the addition of TNFalpha for 4 h and mRNA levels analysed by quantitative reverse-transcription polymerase chain reaction. RESULTS: When human preadipocytes were cultured in a defined medium containing foetal calf serum the Om cells had a greater level of expression of cIAP2 mRNA than Sc cells from the same individual (mean 3.5-fold higher Sc>Om; P<0.01). However, when serum was removed from this media for a transitory period the level of cIAP2 mRNA decreased in the omental depot such that Sc preadipocytes had greater cIAP2 expression than their Om counterparts. Addition of TNFalpha induced a large increase in mRNA levels of cIAP2 (mean 20-fold). CONCLUSIONS: These results demonstrate that cIAP2 is expressed in a depot-specific manner in human preadipocytes and that levels of expression are regulated by serum factors and TNFalpha. Thus there may be intrinsic differences between preadipocyte cells from different adipose depots and this may play a role in the regulation of body fat distribution via the modulation of fat cell apoptosis.

Adipocytes↗
PubMed2003

Historical perspective: visceral obesity and related comorbidity in Joannes Baptista Morgagni's 'De sedibus et causis morborum per anatomen indagata'.

In recent years, advances in epidemiological approaches and laboratory technology, along with the availability of sophisticated imaging methods to evaluate body fat distribution, made it possible to define the close correlation between visceral fat accumulation and the occurrence of metabolic abnormalities, cardiovascular diseases and respiratory disturbances in obese patients. Some 250 y ago, JB Morgagni with the help of only a knife for anatomical dissection, an acute mind, and an observational skillfulness was able to identify the intra-abdominal and mediastinal fat accumulation in android obesity. He clearly described the association between visceral obesity, hypertension, hyperuricemia, atherosclerosis and obstructive sleep apnea syndrome, long before the modern recognition of this syndrome.

Comorbidity↗
PubMed2004

Obesity and impaired fibrinolysis: role of adipose production of plasminogen activator inhibitor-1.

Obesity is the central promoter of the metabolic syndrome which also includes disturbed fibrinolysis in addition to hypertension, dyslipidaemia and impaired glucose tolerance/type 2 diabetes mellitus. Plasminogen activator inhibitor-1 (PAI-1) is the most important endogenous inhibitor of tissue plasminogen activator and uro-plasminogen activator, and is a main determinant of fibrinolytic activity. There is now compelling evidence that obesity and, in particular, an abdominal type of body fat distribution are associated with elevated PAI-1 antigen and activity levels. Recent studies established that PAI-1 is expressed in adipose tissue. The greater the fat cell size and the adipose tissue mass, the greater is the contribution of adipose production to circulating PAI-1. Experimental data show that visceral adipose tissue has a higher capacity to produce PAI-1 than subcutaneous adipose tissue. Studies in human adipocytes indicate that PAI-1 synthesis is upregulated by insulin, glucocorticoids, angiotensin II, some fatty acids and, most potently, by cytokines such as tumour necrosis factor-alpha and transforming growth factor-beta, whereas catecholamines reduce PAI-1 production. Interestingly, pharmacological agents such as thiazolidinediones, metformin and AT(1)-receptor antagonists were found to reduce adipose expression of PAI-1. In addition, weight loss by dietary restriction or comprehensive lifestyle modification is effective in lowering PAI-1 plasma levels. In conclusion, impaired fibrinolysis in obesity is probably also due to an increased expression of PAI-1 in adipose tissue. An altered function of the endocrine system and an impaired auto-/paracrine function at the fat cell levels may mediate this disturbance of the fibrinolytic system and thereby increase the risk for cardiovascular disease..

Adipocytes↗