Novel insight into perirenal adipose tissue: A neglected adipose depot linking cardiovascular and chronic kidney disease

Obesity is associated with adverse metabolic diseases including cardiovascular disease (CVD) and chronic kidney disease (CKD). These obesity-related diseases are highly associated with excess fat accumulation in adipose tissue. However, emerging evidence indicates that visceral adiposity associates more with metabolic and cardiovascular risk factors. Perirenal adipose tissue, surrounding the kidney, is originally thought to provides only mechanical support for kidney. However, more studies demonstrated perirenal adipose tissue have a closer association with renal disease than other visceral fat deposits in obesity. Additionally, perirenal adipose tissue is also an independent risk factor for CKD and even associated more with CVD. Thus, perirenal adipose tissue may be a connection of CVD with CKD. Here, we will provide an overview of the perirenal adipose tissue, a neglected visceral adipose tissue, and the roles of perirenal adipose tissue linking with CVD and CKD and highlight the perirenal adipose tissue as a potential strategy for future therapeutics against obesity-related disease.     

Effects of antidiabetic drugs on epicardial fat

Epicardial adipose tissue is defined as a deposit of adipocytes with pathophysiological properties similar to those of visceral fat, located in the space between the myocardial muscle and the pericardial sac. When compared with subcutaneous adipose tissue, visceral adipocytes show higher metabolic activity, lipolysis rates, increased insulin resistance along with more steroid hormone receptors. The epicardial adipose tissue interacts with numerous cardiovascular pathways via vasocrine and paracrine signalling comprised of pro-and anti-inflammatory cytokines excretion. Both the physiological differences be-tween the two tissue types, as well as the fact that fat distribution and phenotype, rather than quantity, affect cardiovascular function and metabolic processes, establish epicardial fat as a biomarker for cardiovascular and metabolic syndrome. Numerous studies have underlined an association of altered epicardial fat morphology, type 2 diabetes mellitus(T2 DM) and adverse cardiovascular events. In this review, we explore the prospect of using the epicardial adipose tissue as a therapeutic target in T2 DM and describe the underlying mechanisms by which the antidiabetic drugs affect the pathophysiological processes induced from adipose tissue accumulation and possibly allow for more favourable cardiovascular outcomes though epicardial fat manipulation.     

Plasma visfatin concentrations and fat depot-specific mRNA expression in humans

Visceral and subcutaneous adipose tissue display important metabolic differences that underlie the association of visceral obesity with obesity-related cardiovascular and metabolic alterations. Recently, visfatin was identified as an adipokine, which is predominantly secreted from visceral adipose tissue both in humans and mice. In this study, we examined whether visfatin plasma concentrations (using enzyme immunosorbent assay) and mRNA expression (using RT-PCR) in visceral and subcutaneous fat correlates with anthropometric and metabolic parameters in 189 subjects with a wide range of obesity, body fat distribution, insulin sensitivity, and glucose tolerance. Visfatin plasma concentration correlates positively with the visceral visfatin mRNA expression (r(2) = 0.17, P < 0.0001), BMI (r(2) = 0.062, P = 0.004), percent body fat (r(2) = 0.048, P = 0.01), and negatively with subcutaneous visfatin mRNA expression (r(2) = 0.18, P < 0.0001). However, in a subgroup of 73 individuals, in which visceral fat mass was calculated from computed tomography scans, there was no correlation between plasma visfatin concentrations and visceral fat mass. We found no significant correlation between visfatin plasma concentrations and parameters of insulin sensitivity, including fasting insulin, fasting plasma glucose concentrations, and the glucose infusion rate during the steady state of an euglycemic-hyperinsulinemic clamp independent of percent body fat. Visfatin gene expression was not different between visceral and subcutaneous adipose tissue in the entire study group nor in selected subgroups. We found a significant correlation between visceral visfatin gene expression and BMI (r(2) = 0.06, P = 0.001) and percent body fat (measured using dual-energy X-ray absorptiometry) (r(2) = 0.044, P = 0.004), whereas no significant association between BMI or percent body fat and subcutaneous visfatin mRNA expression existed (both P >0.5). In conclusion, visfatin plasma concentrations and visceral visfatin mRNA expression correlated with measures of obesity but not with visceral fat mass or waist-to-hip ratio. In addition, we did not find differences in visfatin mRNA expression between visceral and subcutaneous adipose tissue in humans.     

Differential responses of visceral and subcutaneous fat depots to nutrients

Increased visceral adiposity is a pivotal component of the metabolic syndrome. Differential gene expression patterns of fat-derived peptides (FDPs) in visceral fat and subcutaneous fat have been characterized in the fasting state. Here we examined whether delivery of nutrients differentially affects the expression of FDPs in visceral fat versus subcutaneous fat (in the fed state). We increased the rate of glucose flux into adipose tissue of normal rats (n = 16) by hyperglycemia or hyperinsulinemia using the clamp technique. Glucose uptake was associated with increased expression of FDPs, including resistin ( approximately 5-fold), adiponectin ( approximately 2-fold), leptin ( approximately 15-fold), plasminogen activating inhibitor-1 ( approximately 10-fold), and angiotensinogen ( approximately 4-fold) in visceral fat, but markedly less in subcutaneous fat. Cytokine expression derived mainly from vascular/stromal/macrophage components of adipose tissue was less dramatically increased. Infusion of glucosamine amplified the results obtained by increasing glucose uptake into adipose tissue, suggesting that flux through the hexosamine biosynthetic pathway may serve as a mechanism for "nutrient sensing." Nutrient-dependent expression of FDPs in visceral fat was also associated with increased plasma levels of several FDPs. Because a biologic sensing pathway can dynamically couple daily food intake to abnormal plasma levels of important FDPs, we challenge the practice of obtaining plasma levels after fasting to assess risk factors for metabolic syndrome.     

Dysregulation of the peripheral and adipose tissue endocannabinoid system in human abdominal obesity

The endocannabinoid system has been suspected to contribute to the association of visceral fat accumulation with metabolic diseases. We determined whether circulating endocannabinoids are related to visceral adipose tissue mass in lean, subcutaneous obese, and visceral obese subjects (10 men and 10 women in each group). We further measured expression of the cannabinoid type 1 (CB(1)) receptor and fatty acid amide hydrolase (FAAH) genes in paired samples of subcutaneous and visceral adipose tissue in all 60 subjects. Circulating 2-arachidonoyl glycerol (2-AG) was significantly correlated with body fat (r = 0.45, P = 0.03), visceral fat mass (r = 0.44, P = 0.003), and fasting plasma insulin concentrations (r = 0.41, P = 0.001) but negatively correlated to glucose infusion rate during clamp (r = 0.39, P = 0.009). In visceral adipose tissue, CB(1) mRNA expression was negatively correlated with visceral fat mass (r = 0.32, P = 0.01), fasting insulin (r = 0.48, P < 0.001), and circulating 2-AG (r = 0.5, P < 0.001), whereas FAAH gene expression was negatively correlated with visceral fat mass (r = 0.39, P = 0.01) and circulating 2-AG (r = 0.77, P < 0.001). Our findings suggest that abdominal fat accumulation is a critical correlate of the dysregulation of the peripheral endocannabinoid system in human obesity. Thus, the endocannabinoid system may represent a primary target for the treatment of abdominal obesity and associated metabolic changes.     

Higher Content of <Emphasis Type="Italic">Trans</Emphasis> Fatty Acids in Abdominal Visceral Fat of Morbidly Obese Individuals undergoing Bariatric Surgery compared to Non-Obese Subjects

Background: The purpose of this study was to determine the total content of trans fatty acids (TFA) in subcutaneous, retroperitoneal and visceral fat of morbidly obese and non-obese patients submitted to bariatric surgery or plastic and abdominal surgery. Methods: The adipose tissues were obtained by surgery; lipids were extracted, saponified and esterified. TFA were measured by FTIR-ATR spectroscopy. Results: The TFA average in obese patients was 6.3% for retroperitoneal and 8.7% for visceral fat. For non-obese patients, the figures were 6.9% (subcutaneous) and 9.3% (visceral). There was no difference between the groups. However, the TFA depot in visceral fat was higher than other fatty tissues for morbidly obese (P<0.001) and non-obese (P<0.05) patients. Conclusions: Our values for TFA content in all adipose tissues analyzed are higher than reported in other countries (3-6%). We showed more TFA in visceral adipose tissue than in other abdominal fat (subcutaneous and retroperitoneal) stores. The visceral adipose tissue level is worrisome because the higher rate of lipolysis in this tissue appears to be an important indicator of metabolic alterations and the levels of TFA found in adipose tissue presumably reflect the higher dietary intake of TFA by Brazilians.     

The inflammatory syndrome: the role of adipose tissue cytokines in metabolic disorders linked to obesity

The metabolic effects of obesity have made this highly prevalent disease one of the most common risk factors for diabetes, hypertension, and atherosclerosis, the leading causes of end-stage renal failure. However, obesity per se, as defined by body mass index, is less predictive of the development of these diseases than is the presence of a constellation of obesity-related abnormalities now known as the metabolic syndrome. Recognition of this syndrome, which can readily be identified in clinical settings using defined threshold values for waist circumference, BP, fasting glucose, and dyslipidemia, allows for earlier intervention in these high-risk patients. Systemic insulin resistance has been implicated as one possible factor that links visceral obesity to adverse metabolic consequences; however, the mechanism whereby adipose tissue causes alterations in insulin sensitivity remains unclear. Infection and inflammation are commonly associated with insulin resistance, and visceral obesity is associated with a chronic, low-grade inflammatory state, suggesting that inflammation may be a potential mechanism whereby obesity leads to insulin resistance. Moreover, adipose tissue is now recognized as an immune organ that secretes numerous immunomodulatory factors and seems to be a significant source of inflammatory signals known to cause insulin resistance. Therefore, inflammation within white adipose tissue may be a crucial step contributing to the emergence of many of the pathologic features that characterize the metabolic syndrome and result in diabetes and atherosclerosis. This review describes the role of proinflammatory cytokines and hormones released by adipose tissue in generating the chronic inflammatory profile associated with visceral obesity.     

Additional Effect of Visceral Fat Resection in an Obese Rat Model of Gastric Banding

Background  There is accumulating agreement that bariatric surgery is currently the most efficacious and enduring treatment for clinically severe obesity, and as a result, the number of bariatric surgeries performed worldwide has increased in recent years. Although the function of visceral fat has gradually become clear, the effect of visceral fat resection is still unknown. The aim of this study was to clarify the additional effect of visceral fat resection in an obese rat model of gastric banding. Methods  Forty male Zucker fatty rats were divided into four groups: the control group, visceral fat resection group, gastric banding group, and gastric banding with visceral fat resection group. They were followed for 8 weeks after surgery, and their body weight change, cumulative food intake, metabolic parameters, and adipocytokines were measured. Results  The gastric banding rats either with or without visceral fat resection showed significant decreases in weight gain, cumulative food intake, and levels of metabolic parameters compared to the control rats. There were no significant differences in weight gain and cumulative food intake between gastric banding with and without visceral fat resection. However, gastric banding with visceral fat resection resulted in lower plasma levels of free fatty acid and TNF-alpha compared to gastric banding alone, and expression of adiponectin mRNA in the adipose tissue was significantly decreased with the addition of visceral fat resection compared with banding alone. There were no significant differences in any parameters between controls and rats receiving visceral fat resection alone. Conclusion  Visceral fat resection may improve adipocytokines and free fatty acid in an obese rat model of gastric banding. However, further studies are necessary before the procedure can be considered an option on bariatric surgery.     

Range of adiposity and cardiorenal syndrome

Obesity and obesity-related co-morbidities, diabetes mellitus, and hypertension are among the fastest-growing risk factors of heart failure and kidney disease worldwide. Obesity, which is not a unitary concept, or a static process, ranges from alterations in distribution to the amount of adiposity. Visceral adiposity, which includes intraabdominal visceral fat mass and ectopic fat deposition such as hepatic, cardiac, or renal, was robustly associated with a greater risk for cardiorenal morbidity than subcutaneous adiposity. In addition, morbid obesity has also demonstrated a negative effect on cardiac and renal functioning. The mechanisms by which adipose tissue is linked with the cardiorenal syndrome (CRS) are hemodynamic and mechanical changes, as well neurohumoral pathways such as insulin resistance, endothelial dysfunction, nitric oxide bioavailability, renin-angiotensin-aldosterone, oxidative stress, sympathetic nervous systems, natriuretic peptides, adipokines and inflammation. Adiposity and other associated co-morbidities induce adverse cardiac remodeling and interstitial fibrosis. Heart failure with preserved ejection fraction has been associated with obesity-related functional and structural abnormalities. Obesity might also impair kidney function through hyperfiltration, increased glomerular capillary wall tension, and podocyte dysfunction, which leads to tubulointerstitial fibrosis and loss of nephrons and, finally, chronic kidney disease. The development of new treatments with renal and cardiac effects in the context of type 2 diabetes, which improves mortality outcome, has highlighted the importance of CRS and its prevalence. Increased body fat triggers cellular, neuro-humoral and metabolic pathways, which create a phenotype of the CRS with specific cellular and biochemical biomarkers. Obesity has become a single cardiorenal umbrella or type of cardiorenal metabolic syndrome. This review article provides a clinical overview of the available data on the relationship between a range of adiposity and CRS, the support for obesity as a single cardiorenal umbrella, and the most relevant studies on the recent therapeutic approaches.     

A unique defect in the regulation of visceral fat cell lipolysis in the polycystic ovary syndrome as an early link to insulin resistance.

The etiology of polycystic ovary syndrome (PCOS) is unknown. However, PCOS has a strong resemblance to the insulin resistance (metabolic) syndrome, where an increased rate of visceral fat cell lipolysis is believed to play a pathophysiological role. We hypothesized that primary defects in visceral lipolysis might also exist in PCOS. Ten young, nonobese, and otherwise healthy PCOS women were compared with 13 matched control women. In vitro lipolysis regulation and stoichiometric properties of the final step in lipolysis activation, namely the protein kinase A (PKA)-hormone sensitive lipase (HSL) complex, were investigated in isolated visceral (i.e., omental) fat cells. Body fat distribution and circulating levels of insulin, glucose, and lipids were normal in PCOS women. However, in vivo insulin sensitivity was slightly decreased (P = 0.03). Catecholamine-induced adipocyte lipolysis was markedly (i.e., about twofold) increased in PCOS women due to changes at the postreceptor level, although there was no change in the antilipolytic properties of visceral fat cells. Western blot analyses of visceral adipose tissue showed twofold increased levels of the catalytic and the regulatory Ialpha components of PKA. In contrast, the regulatory RIIbeta component of PKA was almost 50% decreased in visceral adipose tissue in PCOS women. Recent studies on genetically modified mice have shown that a similar transition in the regulatory PKA units induces an increased lipolytic response to catecholamines. Further analysis showed that the level of HSL-short, an enzymatically inactive splice form of HSL, was decreased in PCOS (P < 0.01). The altered lipolysis in PCOS is different from that observed in visceral fat cells in the insulin resistance syndrome that occurs at the level of adrenergic receptors. We concluded that increased catecholamine-induced lipolysis in visceral fat cells may be due to unique alterations in the stoichiometric properties of the adipose PKA-HSL holoenzymes. This could be an early and possibly primary lipolysis defect in PCOS.     

Ex vivo fat graft preservation: effects and implications of cryopreservation

There are a variety of recommended methods for harvesting, treating, and utilizing autologous fat grafts. Previous work with the MTT assay illustrated that various preimplantation handling techniques had minimal effect on the viability of fat samples. This assay was used to test the viability of harvested fat samples after being stored for up to 8 days in a variety of conditions. Surprisingly, freezing the fat before assaying also had no measurable detrimental effect, which led us to study this phenomenon in greater detail. The results demonstrated that fat stored at subzero temperatures showed remarkable maintenance of their mitochondrial metabolic activity as compared with fat stored in a 32 degrees C incubator. These data suggest exciting possibilities for storage and banking of human adipose tissue, which would reduce patient cost, discomfort, and time associated with multiple grafting procedures.     

Omentin plasma levels and gene expression are decreased in obesity

Central obesity and the accumulation of visceral fat are risk factors for the development of type 2 diabetes and cardiovascular disease. Omentin is a protein expressed and secreted from visceral but not subcutaneous adipose tissue that increases insulin sensitivity in human adipocytes. To determine the impact of obesity-dependent insulin resistance on the regulation of two omentin isoforms, gene expression and plasma levels were measured in lean, overweight, and obese subjects. Omentin 1 was shown to be the major circulating isoform in human plasma. Lean subjects had significantly higher plasma omentin 1 levels than obese and overweight subjects. In addition, higher plasma omentin 1 levels were detected in women compared with men. Plasma omentin 1 levels were inversely correlated with BMI, waist circumference, leptin levels, and insulin resistance as measured by homeostasis model assessment and positively correlated with adiponectin and HDL levels. Both omentin 1 and omentin 2 gene expression were decreased with obesity and were highly correlated with each other in visceral adipose tissue. In summary, decreased omentin levels are associated with increasing obesity and insulin resistance. Therefore, omentin levels may be predictive of the metabolic consequences or co-morbidities associated with obesity.     

Intrinsic differences in adipocyte precursor cells from different white fat depots

Obesity and body fat distribution are important risk factors for the development of type 2 diabetes and metabolic syndrome. Evidence has accumulated that this risk is related to intrinsic differences in behavior of adipocytes in different fat depots. In the current study, we demonstrate that adipocyte precursor cells (APCs) isolated from visceral and subcutaneous white adipose depots of mice have distinct patterns of gene expression, differentiation potential, and response to environmental and genetic influences. APCs derived from subcutaneous fat differentiate well in the presence of classical induction cocktail, whereas those from visceral fat differentiate poorly but can be induced to differentiate by addition of bone morphogenetic protein (BMP)-2 or BMP-4. This difference correlates with major differences in gene expression signature between subcutaneous and visceral APCs. The number of APCs is higher in obesity-prone C57BL/6 mice than obesity-resistant 129 mice, and the number in both depots is increased by up to 270% by exposure of mice to high-fat diet. Thus, APCs from visceral and subcutaneous depots are dynamic populations, which have intrinsic differences in gene expression, differentiation properties, and responses to environmental/genetic factors. Regulation of these populations may provide a new target for the treatment and prevention of obesity and its metabolic complications.     

Visceral and subcutaneous adipose tissue,which one induced thyroid dysfunction in patients with morbid obesity

BackgroundThyroid dysfunction in patients with morbid obesity usually resolves after bariatric surgery. However, the role of diverse types of adipose tissue in the process remains unknown.ObjectivesWe aim to investigate the effects of visceral and subcutaneous fat on thyroid function in a Chinese population with morbid obesity who underwent sleeve gastrectomy (SG).SettingUniversity hospital, Shanghai, ChinaMethodsRepeated measurement data of thyroid hormone and body fat were collected at 0, 3, 6, 12, 24, and 36 months after sleeve gastrectomy. Dual-energy X-ray absorptiometer and quantitative computerized tomography (CT) were used to compute visceral fat and subcutaneous fat. Repeated measures correlation (rmmcorr) package was employed for correlation analysis with generalized additive mixed model (GAMM) determining the independent factors.ResultsThyroid stimulating-hormone (TSH) showed notable decrease at 36 months after surgery, coupled with reduction of BMI (38.08 kg/cm² versus 24.28 kg/cm²), C-reactive protein (CRP), visceral adipose tissue (786.74 cm² versus 367.44 cm²), body fat rate, and waistline (118.13 cm versus 100.87 cm). Only visceral fat, diabetes, and CRP proved to be independent variables for TSH decline, without correlation with subcutaneous fat.ConclusionThe present study is first to report the effects of different types of body fat on thyroid function in a Chinese population with morbid obesity, revealing that loss of visceral fat is the key to improving endocrine and metabolic activity after bariatric surgery.     

Noncanonical Wnt Signaling Promotes Obesity-Induced Adipose Tissue Inflammation and Metabolic Dysfunction Independent of Adipose Tissue Expansion

Adipose tissue dysfunction plays a pivotal role in the development of insulin resistance in obese individuals. Cell culture studies and gain-of-function mouse models suggest that canonical Wnt proteins modulate adipose tissue expansion. However, no genetic evidence supports a role for endogenous Wnt proteins in adipose tissue dysfunction, and the role of noncanonical Wnt signaling remains largely unexplored. Here we provide evidence from human, mouse, and cell culture studies showing that Wnt5a-mediated, noncanonical Wnt signaling contributes to obesity-associated metabolic dysfunction by increasing adipose tissue inflammation. Wnt5a expression is significantly upregulated in human visceral fat compared with subcutaneous fat in obese individuals. In obese mice, Wnt5a ablation ameliorates insulin resistance, in parallel with reductions in adipose tissue inflammation. Conversely, Wnt5a overexpression in myeloid cells augments adipose tissue inflammation and leads to greater impairments in glucose homeostasis. Wnt5a ablation or overexpression did not affect fat mass or adipocyte size. Mechanistically, Wnt5a promotes the expression of proinflammatory cytokines by macrophages in a Jun NH₂-terminal kinase–dependent manner, leading to defective insulin signaling in adipocytes. Exogenous interleukin-6 administration restores insulin resistance in obese Wnt5a-deficient mice, suggesting a central role for this cytokine in Wnt5a-mediated metabolic dysfunction. Taken together, these results demonstrate that noncanonical Wnt signaling contributes to obesity-induced insulin resistance independent of adipose tissue expansion.     

Adipose tissue fibrosis

The increasing prevalence of obesity causes a major interest in white adipose tissue biology. Adipose tissue cells are surrounded by extracellular matrix proteins whose composition and remodeling is of crucial importance for cell function. The expansion of adipose tissue in obesity is linked to an inappropriate supply with oxygen and hypoxia development. Subsequent activation of hypoxia inducible factor 1 (HIF-1) inhibits preadipocyte differentiation and initiates adipose tissue fibrosis. Thereby adipose tissue growth is limited and excess triglycerides are stored in ectopic tissues. Stressed adipocytes and hypoxia contribute to immune cell immigration and activation which further aggravates adipose tissue fibrosis. There is substantial evidence that adipose tissue fibrosis is linked to metabolic dysfunction, both in rodent models and in the clinical setting. Peroxisome proliferator activated receptor gamma agonists and adiponectin both reduce adipose tissue fibrosis, inflammation and insulin resistance. Current knowledge suggests that antifibrotic drugs, increasing adipose tissue oxygen supply or HIF-1 antagonists will improve adipose tissue function and thereby ameliorate metabolic diseases.     

The L-α-lysophosphatidylinositol/GPR55 system and its potential role in human obesity

GPR55 is a putative cannabinoid receptor, and l-α-lysophosphatidylinositol (LPI) is its only known endogenous ligand. We investigated 1) whether GPR55 is expressed in fat and liver; 2) the correlation of both GPR55 and LPI with several metabolic parameters; and 3) the actions of LPI on human adipocytes. We analyzed CB1, CB2, and GPR55 gene expression and circulating LPI levels in two independent cohorts of obese and lean subjects, with both normal or impaired glucose tolerance and type 2 diabetes. Ex vivo experiments were used to measure intracellular calcium and lipid accumulation. GPR55 levels were augmented in the adipose tissue of obese subjects and further so in obese patients with type 2 diabetes when compared with nonobese subjects. Visceral adipose tissue GPR55 correlated positively with weight, BMI, and percent fat mass, particularly in women. Hepatic GPR55 gene expression was similar in obese and type 2 diabetic subjects. Circulating LPI levels were increased in obese patients and correlated with fat percentage and BMI in women. LPI increased the expression of lipogenic genes in visceral adipose tissue explants and intracellular calcium in differentiated visceral adipocytes. These findings indicate that the LPI/GPR55 system is positively associated with obesity in humans.     

A review of body mass index and waist circumference as markers of obesity and coronary heart disease risk in persons with chronic spinal cord injury

STUDY DESIGN: Literature review. BACKGROUND: Increased fat mass and coronary heart disease (CHD) are secondary complications of chronic spinal cord injury (SCI). In able-bodied populations, body mass index (BMI, body weight (kg)/height (m(2))) is a widely used surrogate marker of obesity and predictor of CHD risk. Waist circumference, an accurate and reproducible surrogate measure of abdominal visceral adipose tissue, is also associated with CHD risk (more so than BMI) in able-bodied populations. OBJECTIVE: To review the literature on the accuracy of BMI and waist circumference as surrogate measures of obesity and CHD risk in persons with chronic SCI. SETTING: Ontario, Canada. METHODS: Literature review. RESULTS: In the SCI population, BMI is an insensitive marker of obesity, explains less of the variance in measured percent fat mass than in the able-bodied, and is inconsistently related to CHD risk factors. This may be due to potential measurement error, and to the inability of BMI to distinguish between fat and fat-free mass and to measure body fat distribution. Waist circumference has not been validated as a surrogate measure of visceral adipose tissue, however preliminary evidence supports a relationship between waist circumference and CHD risk in the SCI population. CONCLUSIONS: We recommend that SCI-specific BMI classifications be determined. We also recommend that accuracy and reliability of waist circumference as a surrogate measure of visceral adipose tissue and CHD risk be determined in men and women with long-standing paraplegia and tetraplegia.     

代谢异常对结直肠癌发病的影响

代谢异常与结肠癌的发病有关.代谢综合征是一系列代谢异常症候群.目前国际定义的代谢综合征的几个关键因素,如腹型肥胖、血脂异常、血压升高、糖代谢异常,均与结直肠癌的发病相关.腹型肥胖与糖代谢异常可能是影响直肠癌发病的首要因素.在生理学上,内脏脂肪比皮下脂肪更活跃,并且能生成并分泌激素、细胞因子,参与炎症、代谢以及潜在致癌风险,因此,内脏脂肪的多少可能直接或间接地与结直肠癌的发生相关.肥胖可以通过高胰岛素血症、胰岛素样生长因子和脂肪细胞因子浓度的改变等几种机制增加结直肠癌发病的风险.上述代谢标志物不仅能够从病因学上进一步增进对结直肠癌的了解,也能够探索出与结直肠癌发病风险相关的新肥胖表型.