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PubMed2001

Circulating concentrations of the adipocyte protein adiponectin are decreased in parallel with reduced insulin sensitivity during the progression to type 2 diabetes in rhesus monkeys.

Adiponectin is an adipose-specific plasma protein whose plasma concentrations are decreased in obese subjects and type 2 diabetic patients. This protein possesses putative antiatherogenic and anti-inflammatory properties. In the current study, we have analyzed the relationship between adiponectin and insulin resistance in rhesus monkeys (Macaca mulatta), which spontaneously develop obesity and which subsequently frequently progress to overt type 2 diabetes. The plasma levels of adiponectin were decreased in obese and diabetic monkeys as in humans. Prospective longitudinal studies revealed that the plasma levels of adiponectin declined at an early phase of obesity and remained decreased after the development of type 2 diabetes. Hyperinsulinemic-euglycemic clamp studies revealed that the obese monkeys with lower plasma adiponectin showed significantly lower insulin-stimulated peripheral glucose uptake (M rate). The plasma levels of adiponectin were significantly correlated to M rate (r = 0.66, P < 0.001). Longitudinally, the plasma adiponectin decreased in parallel to the progression of insulin resistance. No clear association was found between the plasma levels of adiponectin and its mRNA levels in adipose tissue. These results suggest that reduction in circulating adiponectin may be related to the development of insulin resistance.

Adiponectin↗
PubMed2002

Low plasma adiponectin concentrations do not predict weight gain in humans.

Low concentrations of plasma adiponectin, the most abundant adipose-specific protein, are observed in obese individuals and predict the development of type 2 diabetes. Administration of adiponectin to rodents prevented diet-induced weight gain, suggesting a potential etiologic role of hypoadiponectinemia in the development of obesity. Our aim was to prospectively examine whether low plasma adiponectin concentrations predict future weight gain in Pima Indians, explaining the predictive effect of adiponectin on the development of type 2 diabetes. We measured plasma adiponectin concentrations in 219 nondiabetic Pima Indians (112 M/107 F, age 31 +/- 9 years, body weight 96 +/- 20 kg [mean +/- SD]) in whom body weight and height were measured and BMI calculated at baseline and follow-up. Cross-sectionally, plasma adiponectin concentrations were negatively associated with body weight (r = -0.28, P = 0.0001). Prospectively, plasma adiponectin concentrations at baseline were not associated with change in weight or BMI before or after adjustment for time of follow-up or after additional adjustment for age at follow-up and sex (all P > 0.3). Our data suggest that low plasma adiponectin concentrations do not play an etiologic role in development of obesity in Pima Indians. Therefore, the predictive effect of low plasma adiponectin concentrations on the development of type 2 diabetes seems to be mediated by factors other than increased adiposity.

Adiponectin↗
PubMed2002

The effect of thiazolidinediones on plasma adiponectin levels in normal, obese, and type 2 diabetic subjects.

The insulin-sensitizing effects of thiazolidinediones are thought to be mediated through peroxisome proliferator-activated receptor-gamma, a nuclear receptor that is highly abundant in adipose tissue. It has been reported that adipocytes secrete a variety of proteins, including tumor necrosis factor-alpha, resistin, plasminogen activator inhibitor-1, and adiponectin. Adiponectin is a fat cell-secreted protein that has been reported to increase fat oxidation and improve insulin sensitivity. Our aim was to study the effects of troglitazone on adiponectin levels in lean, obese, and diabetic subjects. Ten diabetic and 17 nondiabetic subjects (8 lean, BMI <27 kg/m(2) and 9 obese, BMI >27 kg/m(2)) participated in the study. All subjects underwent an 80 mU. m(-2). min(-1) hyperinsulinemic-euglycemic glucose clamp before and after 3 months' treatment with the thiazolidinedione (TZD) troglitazone (600 mg/day). Fasting plasma glucose significantly decreased in the diabetic group after 12 weeks of treatment compared with baseline (9.1 +/- 0.9 vs. 11.1 +/- 0.9 mmol/l, P < 0.005) but was unchanged in the lean and obese subjects. Fasting insulin for the entire group was significantly lower than baseline (P = 0.02) after treatment. At baseline, glucose disposal rate (R(d)) was lower in the diabetic subjects (3.4 +/- 0.5 mg. kg(-1). min(-1)) than in the lean (12.3 +/- 0.4) or obese subjects (6.7 +/- 0.7) (P < 0.001 for both) and was significantly improved in the diabetic and obese groups (P < 0.05) after treatment, and it remained unchanged in the lean subjects. Baseline adiponectin levels were significantly lower in the diabetic than the lean subjects (9.0 +/- 1.7 vs. 16.7 +/- 2.7 micro g/ml, P = 0.03) and rose uniformly in all subjects (12.2 +/- 2.3 vs. 25.7 +/- 2.6 micro g/ml, P < 10(-4)) after treatment, with no significant difference detected among the three groups. During the glucose clamps, adiponectin levels were suppressed below basal levels in all groups (10.2 +/- 2.3 vs. 12.2 +/- 2.3 micro g/ml, P < 0.01). Adiponectin levels correlated with R(d) (r = 0.46, P = 0.016) and HDL cholesterol levels (r = 0.59, P < 0.001) and negatively correlated with fasting insulin (r = -0.39, P = 0.042) and plasma triglyceride (r = -0.61, P < 0.001). Our findings show that TZD treatment increased adiponectin levels in all subjects, including normal subjects in which no other effects of TZDs are observed. Insulin also appears to suppress adiponectin levels. We have confirmed these results in normal rats. These findings suggest that adiponectin can be regulated by obesity, diabetes, TZDs, and insulin, and it may play a physiologic role in enhancing insulin sensitivity.

Adiponectin↗
PubMed2002

Androgens decrease plasma adiponectin, an insulin-sensitizing adipocyte-derived protein.

Adiponectin, an adipose-specific secretory protein, exhibits antidiabetic and antiatherogenic properties. In the present study, we examined the effects of sex hormones on the regulation of adiponectin production. Plasma adiponectin concentrations were significantly lower in 442 men (age, 52.6 +/- 11.9 years [mean +/- SD]) than in 137 women (53.2 +/- 12.0 years) but not different between pre- and postmenopausal women. In mice, ovariectomy did not alter plasma adiponectin levels. In contrast, high levels of plasma adiponectin were found in castrated mice. Testosterone treatment reduced plasma adiponectin concentration in both sham-operated and castrated mice. In 3T3-L1 adipocytes, testosterone reduced adiponectin secretion into the culture media, using pulse-chase study. Castration-induced increase in plasma adiponectin was associated with a significant improvement of insulin sensitivity. Our results indicate that androgens decrease plasma adiponectin and that androgen-induced hypoadiponectinemia may be related to the high risks of insulin resistance and atherosclerosis in men.

3T3 Cells↗
PubMed2003

Modulation of circulating and adipose tissue adiponectin levels by antidiabetic therapy.

The relationship between insulin action and control of the adipocyte-derived factor adiponectin was studied in age- and weight-matched obese individuals with type 2 diabetes failing sulfonylurea therapy. After initial metabolic characterization, subjects were randomized to troglitazone or metformin treatment groups; all subjects received glyburide (10 mg BID) as well. Treatment was continued for 3 months. The extent of glycemic control after treatment was similar in both groups. However, the increase in maximal insulin-stimulated glucose disposal rate was greater following troglitazone therapy (+44%) compared with metformin treatment (+20%). Troglitazone treatment increased serum adiponectin levels nearly threefold. There was no change in serum adiponectin with metformin treatment. A positive correlation was found between increases in whole-body glucose disposal rates and serum adiponectin levels after troglitazone; no such relationship was seen with metformin. The adiponectin protein content of subcutaneous abdominal adipocytes was increased following troglitazone treatment and unchanged after metformin. Adiponectin release from adipocytes was also augmented with troglitazone treatment. Adiponectin was present in adipocytes and plasma in several multimeric forms; a trimer was the major form secreted from adipocytes. These results indicate that increases in adiponectin content and secretion are associated with improved insulin action but are not directly related to glycemic control. Modulation of adipocyte function, including upregulation of adiponectin synthesis and secretion, may be an important mechanism by which thiazolidinediones influence insulin action.

Adipocytes↗
PubMed2005

Adiponectin and future coronary heart disease events among men with type 2 diabetes.

Adiponectin, predominantly synthesized in the adipose tissue, seems to have substantial anti-inflammatory properties and to be a major modulator of insulin resistance and dyslipidemia, mechanisms that are associated with an increased atherosclerotic risk in diabetic patients. However, it is unknown whether higher levels of adiponectin are associated with a reduced risk for coronary heart disease (CHD) among diabetic individuals. We investigated the association between plasma adiponectin levels and incidence of CHD among 745 men with confirmed type 2 diabetes in the Health Professionals Follow-up Study. Participants were aged 46-81 years and were free of diagnosed cardiovascular disease at the time of blood draw in 1993/1994. During an average of 5 years of follow-up (3,980 person-years), we identified 89 incident cases of CHD (19 myocardial infarction and 70 coronary artery bypass surgery), confirmed by medical records. Levels of adiponectin were inversely associated with BMI and directly associated with age, alcohol intake, and duration of diabetes (P < 0.05). After adjustment for age, BMI, smoking, alcohol consumption, duration of diabetes, and other lifestyle factors, adiponectin was associated with a decreased risk for CHD events. The multivariate relative risk for CHD for a doubling of adiponectin was 0.71 (95% CI 0.53-0.95). Further adjustment for HDL cholesterol attenuated this association (0.78 [0.57-1.06]). The inverse association between adiponectin and CHD was consistent across strata of aspirin use, family history of myocardial infarction, alcohol consumption, insulin use, duration of diabetes, and levels of HbA(1c), triglycerides, C-reactive protein, and HDL cholesterol. Our study suggests that increased adiponectin levels are associated with a moderately decreased CHD risk in diabetic men. This association seems to be mediated in part by effects of adiponectin on HDL cholesterol levels.

Adiponectin↗
PubMed2003

Adiponectin in a native Canadian population experiencing rapid epidemiological transition.

OBJECTIVE: Adiponectin is emerging as an important protein in the etiology of obesity and related metabolic disorders. The objectives of this study were to determine cross-sectional and prospective associations of adiponectin concentration with adiposity, type 2 diabetes, and cardiovascular disease (CVD) risk factors in a population-based study of Native Canadians, a group experiencing dramatic increases in diabetes and CVD. RESEARCH DESIGN AND METHODS: During the 1993-1995 baseline survey, samples for glucose, insulin, adiponectin, and lipids were collected after an overnight fast. Waist circumference and percent body fat were measured, and a 75-g oral glucose tolerance test was administered: n = 505 with normal glucose tolerance (NGT), 74 with impaired glucose tolerance (IGT), and 149 with diabetes. In 1998, 95 high-risk subjects, defined as those who, at baseline, had either IGT or NGT with an elevated 2-h glucose concentration (>/==" BORDER="0">7.0 mmol/l), participated in a follow-up examination using the protocol used at baseline. RESULTS: After adjustment for covariates including percent body fat and homeostasis model assessment of insulin resistance (HOMA-IR), adiponectin concentrations were significantly lower among men versus women (10.8 vs. 15.0 micro g/ml, P < 0.0001) and among diabetic versus NGT subjects (11.1 vs. 13.1 micro g/ml, P < 0.05). Adiponectin was inversely correlated with percent body fat, waist circumference, HOMA-IR, and triglyceride and positively correlated with HDL (r = |0.30|-|0.44|, all P < 0.0001). In multivariate linear regression analysis in nondiabetic subjects, HDL and percent body fat were significantly related to adiponectin variation among both men and women (R(2) = 28-29%). Factor analysis returned three underlying factors among these variables, with adiponectin loading on the second factor along with insulin, waist circumference, triglyceride, and HDL. In the follow-up study, higher adiponectin at baseline was significantly associated with increases in HDL (r = 0.24, P = 0.03) and decreases in HOMA-IR (r = -0.29, P = 0.009) after adjustment for covariates, including age, adiposity, and diabetes status at baseline and follow-up. CONCLUSIONS: These population-based findings support the hypothesis that low circulating levels of adiponectin are an important determinant of risk of CVD.

Adiponectin↗
PubMed2003

Plasma adiponectin is an independent predictor of type 2 diabetes in Asian indians.

OBJECTIVE: Adiponectin, secreted by fat cells, has regulatory functions on energy metabolism. Its low levels are predictive of future development of diabetes. Because no studies on the regulatory role of adiponectin in glucose homeostasis in Asian Indians exist, this analysis was performed to determine the prospective association of adiponectin and diabetes in subjects with impaired glucose tolerance (IGT). RESEARCH DESIGN AND METHODS: Baseline values of plasma adiponectin, results of anthropometry, fasting and 2-h plasma glucose levels, HbA(1c), results of lipid profile, and insulin resistance were analyzed in 91 subjects with IGT (53 men and 38 women) in a primary prevention study. Reassessment of glucose tolerance was performed during 1-year review. The predictive nature of adiponectin for development of diabetes was assessed using univariate and multiple logistic regression analyses. A control group comprising healthy, normoglycemic individuals was used for comparison. RESULTS: At follow-up, diabetes had developed in 25 of the 91 study subjects. The mean baseline adiponectin level was lower in the diabetic subjects than in the nondiabetic subjects (11.3 +/- 5.5 vs. 16.7 +/- 7.6 micro g/ml, P = 0.0017). Low adiponectin level was a strong predictor of future development of diabetes, and HbA(1c) also showed a positive predictive association. Women had higher adiponectin levels (16.4 +/- 6.1 micro g/ml) than men (13.9 +/- 7.6 micro g/ml) (P = 0.035). CONCLUSIONS: In Asian Indians, low plasma adiponectin level was predictive of future development of diabetes.

Adiponectin↗
PubMed2003

Plasma adiponectin and leptin levels, body composition, and glucose utilization in adult women with wide ranges of age and obesity.

OBJECTIVE: The purpose of this study was to determine the relationships between plasma adiponectin and leptin levels, total and central obesity, and glucose utilization across the adult age span. RESEARCH DESIGN AND METHODS: We studied 148 women aged 18-81 years with a BMI range of 17.2-44.3 kg/m(2). Total percent body fat was determined by dual-energy X-ray absorptiometry and abdominal fat by computed tomography. Glucose tolerance in non-type 2 diabetic volunteers was determined with an oral glucose tolerance test. Glucose utilization (M) was measured during the last 60 min of hyperinsulinemic-euglycemic clamps (240 pmol x m(-2) x min(-1)). Plasma adiponectin levels were measured by radioimmunoassay. The women were separated into three age-groups: young, middle, and old (<40, 40-59, and >or=60 years, respectively), as well as by glucose tolerance status. RESULTS: Adiponectin concentrations did not differ by age-groups. There were significant age effects for BMI, percent body fat, visceral fat, subcutaneous abdominal fat, VO(2max), and M. Adiponectin levels were lower in the prediabetic women (n = 18) than in the normal glucose-tolerant women (n = 108) and the women with type 2 diabetes (n = 22) (both P < 0.05). Univariate correlations revealed significant negative relationships between plasma adiponectin levels and BMI, percent body fat, visceral fat, subcutaneous abdominal fat, fasting leptin, and fasting insulin and positive relationship with M (all P < 0.05). In a multiple stepwise regression model to predict adiponectin, only M remained in the model at P < 0.001. Multivariate analyses revealed a significant relation for M as a function of adiponectin, insulin, and VO(2max). CONCLUSIONS: The data suggest that plasma adiponectin does not change with age but levels are negatively associated with percent body fat, visceral fat, subcutaneous abdominal fat, insulin, and leptin levels in women. Adiponectin is positively associated with M across the age span in women.

Adiponectin↗
PubMed2004

Adiponectin in youth: relationship to visceral adiposity, insulin sensitivity, and beta-cell function.

OBJECTIVE: Adiponectin is an adipose tissue protein that enhances insulin sensitivity and has antiatherogenic properties. The present study investigated the relationship of adiponectin levels in adolescents to 1) obesity and body fat distribution and 2) insulin sensitivity and the components of syndrome X. RESEARCH DESIGN AND METHODS: Twenty-three normal-weight and 26 obese adolescents had fasting adiponectin, lipid profile, and proinsulin measurements performed. Hepatic and peripheral insulin sensitivity were assessed with constant-rate [6,6-(2)H(2)]glucose infusion and a 3-h hyperinsulinemic-euglycemic clamp, respectively. Body composition was evaluated by dual-energy X-ray absorptiometry, and visceral adipose tissue (VAT) and subcutaneous adipose tissue were measured by computed tomography scan at the L(4)-L(5) level. RESULTS: Obese adolescents had approximately 50% lower adiponectin than normal-weight adolescents. Moreover, obese adolescents with high (111.8 +/- 9.3 cm(2)) versus low (55.4 +/- 2.1 cm(2)) VAT had lower adiponectin levels (6.2 +/- 0.9 vs. 9.0 +/- 1.0 microg/ml, P = 0.05). Plasma adiponectin correlated positively with peripheral and hepatic insulin sensitivity (r = 0.67, P < 0.001 and r = 0.54, P < 0.001, respectively) and HDL (r = 0.52, P < 0.001) and negatively with fasting proinsulin and the proinsulin-to-insulin ratio (r = -0.64, P < 0.001 and r = -0.43, P = 0.003, respectively). In a multiple regression analysis, adiponectin, independently and together with BMI, explained 73% (R(2) = 0.73, P < 0.001) of the variance in insulin sensitivity. Adiponectin, but not adiposity, was the significant independent determinant of the proinsulin-to-insulin ratio (R(2) = 0.18, P = 0.008) and of HDL (R(2) = 0.45, P < 0.001). CONCLUSIONS: In summary, hypoadiponectinemia in youth is a strong and independent correlate of insulin resistance, beta-cell dysfunction, visceral adiposity, and syndrome X. The antidiabetogenic and antiatherogenic properties of adiponectin are evident early in life and compromised in youth-onset obesity.

Adiponectin↗
PubMed2004

Relationship between adiponectin and glycemic control, blood lipids, and inflammatory markers in men with type 2 diabetes.

OBJECTIVE: Adiponectin, synthesized in the adipose tissue, appears to play an important role in hyperglycemia and dyslipidemia, as well as in inflammatory mechanisms, which lead to a markedly increased atherosclerotic risk in diabetic subjects. However, previous studies did not evaluate the complex relationships between adiponectin and the array of metabolic abnormalities commonly observed in diabetes. RESEARCH DESIGN AND METHODS: To examine the associations between plasma levels of adiponectin and HbA(1c), blood lipids, and inflammatory markers, we obtained blood samples from 741 participants in the Health Professionals Follow-up Study with a diagnosis of type 2 diabetes. RESULTS: Plasma adiponectin levels were positively correlated with HDL cholesterol and negatively correlated with triglycerides, apolipoprotein B-100 (apoB(100)), C-reactive protein (CRP), and fibrinogen. These associations were not appreciably altered after controlling for lifestyle exposures, medical conditions, and obesity-associated variables. A 10-microg/ml higher level of plasma adiponectin was associated with lower HbA(1c) (-0.21% points, P = 0.001), triglycerides (-0.39 mmol/l, P < 0.001), apoB(100) (-0.04 g/l, P < 0.001), CRP (-0.51 mg/l, P = 0.003), and fibrinogen (-0.53 micromol/l, P < 0.001) and higher HDL cholesterol (0.13 mmol/l, P < 0.001). Associations between adiponectin and inflammatory markers were furthermore independent of HbA(1c) and HDL cholesterol, suggesting that the anti-inflammatory properties of adiponectin are not mediated by potential effects on glycemic control and blood lipids. Our results were consistent among obese and nonobese men. CONCLUSIONS: Our study supports the hypothesis that increased adiponectin levels might be associated with better glycemic control, better lipid profile, and reduced inflammation in diabetic subjects. Measures that increase adiponectin levels might be valuable targets for decreasing the atherosclerotic risk present in diabetes.

Adiponectin↗
PubMed2004

Possible impairment of transcardiac utilization of adiponectin in patients with type 2 diabetes.

OBJECTIVE: Adiponectin, an adipocyte-derived protein, has been suggested to enhance insulin sensitivity and prevent atherosclerosis. Circulating adiponecin levels are reduced in states of insulin resistance such as type 2 diabetes. We examined transcardiac utilization of adiponectin in patients with and without type 2 diabetes. RESEARCH DESIGN AND METHODS: A total of 17 male type 2 diabetic patients and 17 male nondiabetic patients were investigated. Venous blood samples were taken to measure glucose and lipid variables. Blood samples for the measurement of adiponectin were collected simultaneously from the aortic root and coronary sinus. Angiographic semiquantitative stenosis score of coronary artery was also evaluated. RESULTS: The adiponectin levels in both the aortic root and coronary sinus in the diabetic patients were significantly lower than those in the nondiabetic patients. The adiponectin level was significantly lower in the coronary sinus than in the aortic root in the nondiabetic patients, but there was no significant difference between adiponectin levels in the aortic root and coronary sinus in the diabetic patients. The total stenosis score, as an index of severity of coronary artery stenosis, was significantly higher in the diabetic patients than in the nondiabetic patients. The stenosis score was correlated with the degree of transcardiac utilization of adiponectin from the aortic root to coronary sinus in the nondiabetic patients but not in the diabetic patients. CONCLUSIONS: Diabetic patients not only have a decreased adiponectin level in the basal state compared with nondiabetic patients but also have impaired utilization of adiponectin in the coronary artery and/or the heart, which may promote the development of atherosclerosis.

Adiponectin↗
PubMed2005

Plasma adiponectin and insulin resistance in Korean type 2 diabetes mellitus.

Insulin resistance, which implies impairment of insulin signaling in the target tissues, is a common cause of type 2 diabetes. Adipose tissue plays an important role in insulin resistance through the dysregulated production and secretion of adipose-derived proteins, including tumor necrosis factor-alpha, plasminogen activator inhibitor-1, leptin, resistin, angiotensinogen, and adiponectin. Adiponectin was estimated to be a protective adipocytokine against atherosclerosis, and also to have an anti-inflammatory effect. In this study, the relationship between fasting plasma adiponectin concentration and adiposity, body composition, insulin sensitivity (ITT, HOMAIR, QUICK), lipid profile, fasting insulin concentration were examined in Korean type 2 diabetes. The difference in the adiponectin concentrations was also examined in diabetic and non-diabetic subjects, with adjustment for gender, age and body mass index. 102 type 2 diabetics and 50 controls were examined. After a 12-h overnight fast, all subjects underwent a 75 gram oral glucose tolerance test. Baseline blood samples were drawn for the determinations of fasting plasma glucose, insulin, adiponectin, total cholesterol, triglyceride, LDL-cholesterol, and HDL-cholesterol. The body composition was estimated using a bioelectric impedance analyzer (Inbody 2.0). The insulin sensitivity was estimated using the insulin tolerance test (ITT), HOMAIR and QUICK methods. In the diabetic group, the fasting adiponectin concentrations were significantly lower in men than in women. They were negatively correlated with BMI (r=-0.453), hip circumference (r=-0.341), fasting glucose concentrations (r=-0.277) and HOMAIR (r= -0.233). In addition, they were positively correlated with systolic blood pressure (r=0.321) and HDL-cholesterol (r= 0.291). The systolic blood pressure and HDL-cholesterol were found to be independent variables, from a multiple logistic regression analysis, which influenced the adiponectin concentration. Compared with the non-diabetic group, the adiponectin concentrations were significantly lower in the diabetic group, with the exception of obese males. In conclusion, the plasma adiponectin concentrations were closely related to the insulin resistance parameters in Korean type 2 diabetic patients.

Adiponectin↗
PubMed2000

Adiponectin, a new member of the family of soluble defense collagens, negatively regulates the growth of myelomonocytic progenitors and the functions of macrophages.

We investigated the functions of adiponectin, an adipocyte-specific secretory protein and a new member of the family of soluble defense collagens, in hematopoiesis and immune responses. Adiponectin suppressed colony formation from colony-forming units (CFU)-granulocyte-macrophage, CFU-macrophage, and CFU-granulocyte, whereas it had no effect on that of burst-forming units-erythroid or mixed erythroid-myeloid CFU. In addition, adiponectin inhibited proliferation of 4 of 9 myeloid cell lines but did not suppress proliferation of erythroid or lymphoid cell lines except for one cell line. These results suggest that adiponectin predominantly inhibits proliferation of myelomonocytic lineage cells. At least one mechanism of the growth inhibition is induction of apoptosis because treatment of acute myelomonocytic leukemia lines with adiponectin induced the appearance of subdiploid peaks and oligonucleosomal DNA fragmentation. Aside from inhibiting growth of myelomonocytic progenitors, adiponectin suppressed mature macrophage functions. Treatment of cultured macrophages with adiponectin significantly inhibited their phagocytic activity and their lipopolysaccharide-induced production of tumor necrosis factor alpha. Suppression of phagocytosis by adiponectin is mediated by one of the complement C1q receptors, C1qRp, because this function was completely abrogated by the addition of an anti-C1qRp monoclonal antibody. These observations suggest that adiponectin is an important negative regulator in hematopoiesis and immune systems and raise the possibility that it may be involved in ending inflammatory responses through its inhibitory functions. (Blood. 2000;96:1723-1732)

Adiponectin↗
PubMed2005

Single Nucleotide Polymorphisms in exon 3 of the adiponectin gene in subjects with type 2 diabetes mellitus.

PURPOSE: Adiponectin (APM1)--a newly discovered adipocytokine secreted by fat tissue--was recently suggested to play a role in the genetic predisposition to type 2 diabetes, obesity and insulin resistance. Adiponectin gene is localized on chromosome 3q27 within the region which was identified as susceptibility locus for type 2 diabetes and metabolic syndrome. Till now genetic associations of two SNP in exon 2 (+45T/G) and intron 2 (+276G/T) of adiponectin gene with type 2 diabetes and adiponectin level were reported in Japanese population and with insulin resistance in some Caucasian populations (Italy, Germany). Moreover, in the proximal promoter region of the APM1 gene: SNP-11426A/G and -11391A/-11377G haplotype predicted the associations with fasting plasma glucose, type 2 diabetes and adiponectin levels. On the other hand the role of mutations in exon 3 of the adiponectin gene is not so well studied. MATERIAL AND METHODS: The aim of our study was the screening for rare mutation in exon 3 of adiponectin gene in the Polish subjects with type 2 diabetes as there is no data available about the frequency and role of these mutations in our population. The study was performed in the group of 187 Polish origin patients with type 2 diabetes (32 female and 155 male, mean age 54.1 +/- 8.6 yrs) and 102 age and sex matched healthy controls. RESULTS: The frequency of adiponectin gene mutations in exon 3 was 3.9%, while in the control group 0.98% and this difference was not statistically significant. We also observed that adiponectin level is significantly lower in patients with c.331 T-->C mutation (Y111H) in comparison to subjects without this mutation (5.0 ug/ml vs 14.4 ug/ml, p=0.0148). CONCLUSIONS: To our knowledge the present study is the first which shows that in Polish populations.

Adiponectin↗
PubMed2005

Decreased levels of plasma adiponectin in prediabetes, Type 2 diabetes and coronary artery disease.

BACKGROUND: Adiponectin, an adipocyte-derived hormone is implicated in insulin resistance and atherosclerosis. The aim of our study is to compare the levels of adiponectin in subjects with prediabetes and diabetes with subjects with normal glucose. MATERIAL/METHODS: In a cross sectional study, we measured adiponectin and insulin in addition to fasting lipid panel and glucose in 28 subjects with prediabetes, 28 subjects with normal fasting glucose and 33 subjects with type 2 diabetes. RESULTS: Adiponectin levels negatively correlate with insulin resistance index (r = -32.7). There is a significant difference in the levels of adiponectin between subjects with prediabetes and normal fasting glucose. There is a significant difference in adiponectin levels in subjects with prediabetes with Coronary artery disease (CAD) compared to those without CAD (10.24+/-1.02 vs. 7.02+/-0.92 with p<0.01). There is a significant difference in adiponectin levels in subjects with CAD compared to those without coronary artery disease (9.94+/-1.02 vs. 5.02+/-0.82 with p<0.01). CONCLUSIONS: We conclude that decreased plasma adiponectin and insulin resistance coexist in subjects with prediabetes, diabetes and atherosclerosis. Adiponectin concentration is an independent correlate of insulin resistance and atherosclerosis.

Adiponectin↗
PubMed2005

[Serum adiponectin levels in patients with acromegaly].

UNLABELLED: Acromegaly is frequently associated with impaired glucose tolerance or diabetes. Insulin resistance has been reported to be related to low levels of adiponectin, which is exclusively produced by adipose tissue, as well as to decreased concentration of sex hormone binding globuline (SHBG). Growth hormone (GH) excess is associated with increased muscle mass and decreased fat mass. Influence of GH on production and secretion of adiponectin is not completely understood. The aims of this study were to assess serum adiponectin levels in patients with active acromegaly and to compare them with concentrations in the control group and to investigate relationships between adiponectin and indexes: body mass index (BMI) and waist-to-hip ratio (WHR) as well as SHBG levels. MATERIALS AND METHODS: Serum adiponectin and SHBG levels were measured by radioimmunoassay in 30 patients with active acromegaly and in 22 sex-, age-, BMI- and WHR-matched controls. The groups were comparable in prevalence of hypertension and disturbances of glucose metabolism. RESULTS: Serum adiponectin concentrations were higher in acromegalic patients compared with control group (24.03 +/- 9.85 mg/ml vs. 14.46 +/- 3.96 mg/ml, p<0.001). When the subjects were fallen into two groups according to sex, significant differences were also observed. Serum SHBG levels were lower in cases compared with controls (25.36 +/- 22.89 nmol/l vs. 33.54 +/- 15.07 nmol/l, p=0.03). In the control group we found adiponectin positively correlated with SHBG concentrations (r=0.53, p=0.01) and negatively correlated with BMI (r=-0.52, p=0.02) and WHR (r=-0.51, p=0.03). However, these relationships were not observed in patients with acromegaly. No significant associations were found between adiponectin and GH or IGF-I. CONCLUSIONS: Serum concentration of adiponectin is significantly higher in patients with acromegaly when compared with the control group and is independent of BMI, WHR and SHBG. The results suggest that adiponectinemia does not directly affect development of insulin resistance in acromegaly.

Acromegaly↗
PubMedDate not supplied

The relation of serum adiponectin and leptin levels to metabolic syndrome in women before and after the menopause.

INTRODUCTION: It is well known that there is a higher prevalence of cardiovascular risk factors and metabolic syndrome (MS) in postmenopausal women. Recently it has become evident that adiponectin and leptin secreted by adipose tissue may be involved in the pathophysiology of MS. THE AIM OF THE STUDY: was to assess the effects of the menopause on the relationships between adiponectin and leptin and different cardiovascular and metabolic risk factors. MATERIALS AND METHODS: A total of 56 postmenopausal women and 75 premenopausal subjects were enrolled in this study. We measured blood pressure, BMI, waist circumference and WHR, triglycerides (TG), high density lipoprotein cholesterol (cHDL) levels and fasting glucose and applied the oral glucose tolerance test (OGTT). Women were categorised as having 0, 1, 2, 3 or more risk factors. The presence of at least 3 abnormalities was defined as MS. Serum was assayed for adiponectin and leptin by the radioimmunoassay (RIA) method. RESULTS: A decline in adiponectin was related to an increased number of MS variables in postmenopausal and premenopausal women. Postmenopausal women with MS had significantly lower adiponectin concentrations than premenopausal women with MS. Serum adiponectin concentrations were inversely correlated to leptin in postmenopausal women. In premenopausal women no clear relationships were found between serum leptin and the number of metabolic disturbances. In contrast to young women, postmenopausal women showed an increase in leptin secretion with a growing number of MS elements. Compared to premenopausal women with MS, postmenopausal women with MS had higher levels of leptin. We found associations between leptin and different risk factors, mainly in the postmenopausal group. When the presence of MS was used as a dependent variable (yes/no) and adiponectin, leptin and menopause status as independent factors, adiponectin and leptin remained significant variables related to MS. CONCLUSION: The significant role of adiponectin in the pathophysiology of MS in premenopausal and postmenopausal women is confirmed in this study. Leptin is correlated with several MS components but this adipocytokine appears to play a role only in postmenopausal women.

Adiponectin↗