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PubMed2004

Sex-related differences between adiponectin and insulin resistance in schoolchildren.

OBJECTIVE: To study the effect of body composition and adiponectin on insulin resistance and beta-cell function in schoolchildren during puberty. RESEARCH DESIGN AND METHODS: Plasma adiponectin level and its relationships with insulin sensitivity and beta-cell function were analyzed in 500 randomly recruited nondiabetic Taiwanese schoolchildren (245 boys and 255 girls) aged 6-18 years in a national survey program for diabetes in 1999. Insulin resistance and beta-cell function were evaluated by homeostasis model assessment (HOMA). Plasma adiponectin concentrations were determined with radioimmunoassay. RESULTS: Plasma glucose levels remained stable, whereas insulin resistance increased with a compensatory rise in beta-cell function during this period. A transient drop of adiponectin level with a trough at 10-12 years was found in boys but not in girls. This pubertal drop of adiponectin levels in boys coincides with the sharp rise in testosterone concentration. A negative correlation between testosterone levels and adiponectin concentration was also noted in boys (r = -0.142, P = 0.032). Plasma adiponectin levels correlated inversely with relative body weight, fasting insulin concentrations, and insulin resistance index by HOMA in boys aged 15-18 years and in girls aged 11-14 years. No association was observed between adiponectin levels and beta-cell function by HOMA. CONCLUSIONS: There is a transient drop in the level of adiponectin during male puberty, correlated with the increase in testosterone level in boys. Plasma adiponectin levels were inversely correlated with obesity and insulin resistance in boys and girls during the pubertal period.

Adiponectin↗
PubMed2005

Dietary glycemic index, glycemic load, cereal fiber, and plasma adiponectin concentration in diabetic men.

OBJECTIVE: Adiponectin may improve insulin sensitivity, reduce inflammation, and ameliorate glycemic control. However, few studies have evaluated dietary predictors of plasma adiponectin levels, especially among subjects with type 2 diabetes. RESEARCH DESIGN AND METHODS: To examine the associations of dietary glycemic load, glycemic index, and fibers with plasma adiponectin levels, we conducted a cross-sectional analysis in 780 diabetic men from the Health Professionals' Follow-up Study. Dietary information was obtained in 1986, 1990, and 1994 using semiquantitative food-frequency questionnaires. RESULTS: After adjustment for age, BMI, smoking, alcohol consumption, physical activity, aspirin use, HbA(1c), history of hypertension or hypercholesterolemia, and fiber intake, dietary glycemic index and glycemic load were inversely associated with plasma adiponectin in a dose-dependent fashion (P for trend = 0.005 for glycemic index and 0.004 for glycemic load). Adiponectin levels were 13% lower in the highest quintile of dietary glycemic index than in the lowest quintile. For dietary glycemic load, adiponectin levels were 18% lower in the highest quintile than in the lowest. In contrast, high intake of cereal fiber was associated with increased plasma adiponectin levels, adjusting for lifestyle factors and dietary glycemic load (P for trend = 0.003). Adiponectin levels were 19% higher in the highest quintile than in the lowest quintile. Higher magnesium intake was also associated with increased plasma adiponectin. CONCLUSIONS: Diets low in glycemic load and high in fiber may increase plasma adiponectin concentrations in diabetic patients.

Adiponectin↗
PubMed2006

Racial differences in adiponectin in youth: relationship to visceral fat and insulin sensitivity.

OBJECTIVE: The purpose of this study was to investigate 1) whether adiponectin is associated with insulin sensitivity independent of visceral adipose tissue in African-American and Caucasian youth and 2) whether adiponectin is associated with racial differences in insulin sensitivity. RESEARCH DESIGN AND METHODS: Total body fat was measured by dual-energy X-ray absorptiometry and abdominal adipose tissue with computed tomography. Insulin sensitivity was measured by a 3-h hyperinsulinemic-euglycemic clamp. RESULTS: Adiponectin was inversely associated (P < 0.01) with visceral adipose tissue, fasting insulin, and proinsulin and was positively related (P < 0.01) to insulin sensitivity after controlling for Tanner stage and sex independent of race. Stepwise multiple regression revealed that adiponectin was a strong independent predictor of insulin sensitivity, explaining 27% of the variance in insulin sensitivity. When subjects were categorized into tertiles of visceral adipose tissue and further low (< or = 50th) and high (>50th) adiponectin groups, insulin sensitivity was significantly different across the visceral adipose tissue groups (main effect, P < 0.01) in both races. However, within each visceral adipose tissue group, subjects with high adiponectin had higher insulin sensitivity (main effect, P < 0.05) than subjects with low adiponectin, independent of race. Racial differences in insulin sensitivity remained significant (P < 0.01) after controlling for leptin and visceral adipose tissue but not (P > 0.05) after additional adjustment for adiponectin. CONCLUSIONS: Adiponectin is associated with insulin sensitivity independent of visceral adipose tissue in both African-American and Caucasian youth. Low adiponectin in African-American youth may be a biological marker that predisposes them to a greater risk of insulin resistance.

Adiponectin↗
PubMed2003

Association of serum adiponectin levels with breast cancer risk.

PURPOSE: Adiponectin is a peptide hormone secreted from the adipose tissue, affecting the proliferation and insulin sensitivity of various types of cells. Because association of obesity with breast cancer risk is well established, it is possible that adiponectin plays some role in the development of breast cancer. Thus, in the present study, the association of the serum adiponectin levels with breast cancer risk was investigated. EXPERIMENTAL DESIGN: A case-control study was conducted on 102 breast cancer patients (cases) and 100 healthy women (controls). The serum adiponectin levels of cases and controls were examined in their association with breast cancer risk after adjustment for the various classical risk factors (family history, age at menarche, parity, body mass index, and so forth). In addition, the relationship between the serum adiponectin levels and the various clinicopathological characteristics of breast cancers was studied. RESULTS: Women in the low tertile of serum adiponectin levels were associated with a significantly (P < 0.005) increased risk for breast cancer compared with women in the high tertile [odds ratio (OR), 3.63; 95% confidence interval (CI), 1.61-8.19]. Such an association was observed both in the premenopausal women (OR, 3.46; 95% CI, 0.89-13.50) and in the postmenopausal women (OR, 3.90; 95% CI, 1.23-12.44). The frequency of large (>2 cm) tumors and that of high histological grade (2+3) tumors were significantly (P < 0.005 and P < 0.05, respectively) higher in breast cancer patients in the low tertile of the serum adiponectin levels than those in the high and intermediate tertiles. CONCLUSIONS: These results suggest that the low serum adiponectin levels are significantly associated with an increased risk for breast cancer and that tumors arising in women with the low serum adiponectin levels are more likely to show a biologically aggressive phenotype. The association between obesity and breast cancer risk might be partly explained by adiponectin.

Adiponectin↗
PubMed2004

[The rhythmicity of adiponectin and its relation with glucocorticoids, insulin and leptin].

OBJECTIVE: To investigate the circadian rhythmicity of adiponectin in patients with Cushing's syndrome and obesity, as well as in normal subjects. The effects of glucocorticoids, insulin and leptin on the secretion of adiponectin were also explored. METHODS: 15 patients with Cushing's syndrome and 10 with obesity as well as 9 normal subjects were recruited and their serum adiponectin, glucocorticoids, insulin and leptin levels were determined 6 times a day (8:00, 12:00, 16:00, 20:00, 24:00, 3:00). RESULTS: Circadian rhythmicity of adiponectin was not observed, but the adiponectin levels in patients with obesity were lower than those in the normal subjects at all 6 time spots. The area under curve (AUC) of serum adiponectin concentrations were significantly negatively correlated with body mass index (BMI, r = 0.46, P < 0.01), waist circumference (r = -0.33, P < 0.05) and insulin AUC (r = -0.36, P < 0.05). A multiple linear regression analysis revealed that BMI and waist circumference were two significant independent parameters of the plasma adiponectin level. The adiponectin levels did not manifest any change after short term dexamethasone administration with both high and low doses, but were obviously decreased after surgery. CONCLUSIONS: Neither long-term endogenous hyperglucocorticoidism nor short-term dexamethasone administration affects the serum adiponectin levels and the serum adiponectin concentrations remain unchanged even with elevated postprandial insulin levels.

Adiponectin↗
PubMed2005

Plasma adiponectin and gastric cancer.

BACKGROUND: Recently, increased body weight has been associated with an increased risk of cancers at multiple specific sites, including gastric cancer. Adiponectin is a peptide hormone secreted by adipose tissue, affecting the proliferation and insulin sensitivity of various types of cells. Moreover, the circulating level of adiponectin has been reported to be inversely related to body mass index. METHODS: Fasting plasma levels of adiponectin were determined in 75 patients with gastric cancer and 52 healthy controls using an ELISA. In these patients, we analyzed the association between plasma adiponectin level and gastric cancer risk as well as various clinicopathologic characteristics. RESULTS: Plasma adiponectin level was significantly lower in patients with gastric cancer than in healthy controls (9.1 +/- 6.2 versus 13.3 +/- 9.4 ng/mL, P < 0.01) and showed a significant modest inverse relation with the gastric cancer (odds ratio, 0.92; 95% confidence interval, 0.85-0.97; adjusted odds ratio, 0.89; 95% confidence interval, 0.84-0.95], although body mass index was not different. In addition, adiponectin level was extremely low in patients with upper gastric cancers (upper, 5.5 +/- 4.1 ng/mL; middle, 9.7 +/- 6.4 ng/mL; lower, 10.7 +/- 4.1 ng/mL; P = 0.012). Furthermore, adiponectin level tended to decrease as the tumor stage increased (stage I, 9.9 +/- 6.9 ng/mL; stage II, 8.7 +/- 5.5 ng/mL; stage III, 8.6 +/- 4.1 ng/mL; stage IV, 5.2 +/- 6.2 ng/mL; P = 0.34). Interestingly, in 32 patients with undifferentiated cancer, serum adiponectin showed a negative correlation with pathologic findings such as tumor size, depth of invasion, as well as tumor stage (P < 0.05), but no correlation in the remaining 43 patients with differentiated cancer. CONCLUSIONS: Our results suggest that a low plasma adiponectin level is associated with an increased risk for gastric cancer and raise the possibility that adiponectin has a potential role in the progression of gastric cancer, especially in undifferentiated type cancers in the upper stomach.

Adenocarcinoma↗
PubMed2006

Adiponectin as a biomarker of clinical manifestation of metabolic syndrome.

OBJECTIVES: To search whether there are differences in serum levels of adiponectin in subjects with metabolic syndrome (MS) as compared to the healthy controls. METHODS: Serum levels of adiponectin were measured by ELISA in 22 subjects with MS (MS group: 9 males and 13 females, average age +/- SD 43.19 +/- 6.16) and in 17 healthy controls of about the same age (CONT group: 8 males and 9 females, average age +/- SD 45.88 +/- 11.6). All subjects of MS group had BMI >30 and also other criteria of MS (e.g. obesity, insulin resistance, possible disorders of glucose metabolism, dyslipidemia and hypertension) were manifested in all of them. Adiponectin levels in serum were compared between the groups and also within the pooled MS plus CONT group the interrelations between serum levels of adiponectin and BMI, serum fasting insulin (estimated by RIA method) and smoking were examined. For statistical processing one way ANOVA or its non-parametric parallel (Kruskal-Wallis one-way analysis) as well as regression and correlation analysis were used. RESULTS: Subjects with MS syndrome had significantly higher BMI, systolic and diastolic BP, fasting glycemia and insulin level. Significantly higher were also the values of both indexes of insulin resistance such as IR(HOMA) and IR(QUlCKI). In contrast, however, MS group had significantly lower adiponectin level than CONT group. There was no difference between the average age of both groups. In pooled MS plus CONT group inverse correlations were found between serum levels of adiponectin on one side and BMI and fasting insulin level on the other, while the level of adiponectin between smokers (which was declared by 18/39 subjects) and non-smokers did not show any influence on serum levels of adiponectin. CONCLUSIONS: Low level of adiponectin in obese individuals may be considered as a marker predicting a possibility of the development of metabolic syndrome. It is suggested that early regulation of serum adiponectin levels in obese subjects by treatment of obesity, especially in young ones, could result in a lowering the risk of mainly cardiovascular diseases associated with MS.

Adiponectin↗
PubMed2006

Association of adipocytokines (leptin, adiponectin TNF-alpha), insulin and proinsulin with diabetes--the Mumbai Obesity Project [MOP].

Asian Indians have a unique phenotype characterized by increased abdominal obesity and visceral fat despite low body mass index [BMI]. Though studies have indicated some adipocytokines to be associated with diabetes and obesity in Indians, there are virtually no studies relating adipocytokines and proinsulin with diabetes and obesity in Asian Indians. In this study we looked at adipocytokines--leptin, adiponectin and tumour necrosis factor-a [TNF-alpha] and insulin and proinsulin in subjects with diabetes and obesity. Thirty five diabetic subjects and 50 healthy controls were recruited for the study. Leptin [p=0.002J and adiponectin levels [p=0.011] were lower and proinsulin values higher [p<0.001] in diabetic subjects compared to non-diabetic subjects. In addition, leptin [p<0.001] and proinsulin [p<0.001] were higher and adiponectin [p<0.001] lower, in obese subjects compared to non-obese subjects. TNF-alpha failed to show any significant difference between the study groups. Leptin and proinsulin showed a significant and positive correlation with BMI [p<0.001] and waist circumference [p<0.001]. Adiponectin showed an inverse correlation with BMI [p=0.050] and waist circumference [p=0.002]. Proinsulin showed a significant negative association with adiponectin [p=0.002]. Logistic regression analysis revealed leptin to be negatively associated [Odds ratio [OR]: 0.864, 95% confidence interval [95% CI]: 0.775 -0.963, p=0.008] and proinsulin [OR: 1.567, 95% CI: 1.246-1.971, p<0.001] to be positively associated with diabetes even after adjusting for age, gender and BMI. Leptin [OR: 1.365, 95% CI: 1.170-1.592, p<0.001] and proinsulin [OR: 1.617, 95% CI: 1.218 -2.147, p=0.001] showed a significant positive association with obesity, while adiponectin [OR: 0.927, 95% CI: 0.865 - 0.995, p=0.035] had a significant inverse association. Linear regression analysis revealed that adiponectin is inversely associated with proinsulin even after the addition of age, gender and diabetes status [beta= -0.61, p=0.033] into the model. In conclusion, in urban Asian Indians in western India, proinsulin levels showed a positive association, while leptin and adiponectin showed a negative association with diabetes. With regard to obesity, leptin and proinsulin had a positive association, while adiponectin had a negative association. Proinsulin levels showed an inverse association with adiponectin indicating a possible link between insulin secretion and insulin resistance.

Adiponectin↗
PubMedDate not supplied

Adiponectin in patients with obstructive sleep apnea syndrome: course and physiological relevance.

BACKGROUND: Adiponectin is an adipocyte-derived hormone with anti-inflammatory and insulin-sensitizing properties. Insulin resistance is a typical feature of the obstructive sleep apnea syndrome (OSAS). OBJECTIVES: Since nasal continuous positive airway pressure (nCPAP) treatment improves insulin sensitivity in patients with OSAS, we investigated serum adiponectin levels before and during nCPAP treatment to clarify possible interactions between the adiponectin levels and insulin sensitivity in patients with OSAS. METHODS: Thirty nondiabetic, obese patients with OSAS (mean age 56.4 +/- 11.1 years; apnoea-hypopnoea index (AHI) 46.03 +/- 19.57) underwent CPAP treatment. Adiponectin levels and the levels of proinflammatory cytokines and proteins reflecting platelet activation [regulated on activation normally T cell expressed and secreted (RANTES) and soluble P-selectin (sCD62p)], as well as the insulin sensitivity index were measured before, and after 2 days and 3 months of CPAP treatment. RESULTS: Insulin sensitivity increased significantly under nCPAP treatment, whereas adiponectin levels decreased after 2 days of nCPAP treatment, but returned to baseline levels after 3 months of nCPAP treatment. The increase in insulin sensitivity was more pronounced in patients with the highest adiponectin levels at baseline (p = 0.021) after adjustment for body fat (p = 0.003). During treatment, changes in adiponectin levels were highly predictable by the insulin sensitivity index. CONCLUSIONS: We found a significant relation between adiponectin and the insulin sensitivity index in overweight patients with OSAS. The lack of a long-lasting change in adiponectin may be explained by the overwhelming influence of the body mass index on adiponectin secretion, which was unchanged during nCPAP treatment.

Aged↗
PubMed2006

Evidence for a protective role for adiponectin in osteoarthritis.

Obesity has been associated with an increased risk of osteoarthritis (OA). However, the mechanism by which obesity contributes to OA remains uncertain. Adiponectin, an adipocyte-derived hormone, has shown anti-diabetic and anti-atherogenic properties. In the present study, we aimed to investigate the potential role of adiponectin in OA disease. We demonstrated that adiponectin was present in OA synovial fluid (SF) and its expression level was almost 100-fold decrease compared with that in OA plasma. FPLC and ELISA studies revealed the distribution and abundance of the adiponectin complexes in plasma and SF from patients with OA. The percentage of high molecular weight (HMW) per total adiponectin in OA SF was lower than in OA plasma, while that of the hexamer form was similar and the trimer form was higher. The expression levels of adiponectin receptors AdipoR1 and AdipoR2 were examined in human OA tissues by RT-PCR. AdipoR1 was abundantly expressed in cartilage, bone and synovial tissues, whereas AdipoR2 was rarely detected. Finally, the effects of adiponectin on primary chondrocyte functions were studied by using antibody-based protein array and RT-PCR. The patterns of mRNA expression and protein production strongly indicate that adiponectin is involved in the modulation of cartilage destruction in chondrocytes by up-regulating TIMP-2 and down-regulating IL-1beta-induced MMP-13. Together these findings clearly indicate that the adiponectin may act as a protective role in the progression of OA, and this also provide new thinking on the relationship between obesity and OA.

Adiponectin↗
PubMed2005

Adiponectin receptor 2 expression in liver and insulin resistance in db/db mice given a beta3-adrenoceptor agonist.

Our aim was to determine the effect of a beta3-adrenoceptor agonist on plasma adiponectin levels and on the level of expression of mRNA for adiponectin, adiponectin receptor 1, and adiponectin receptor 2 in db/db mice. Two weeks' oral administration of CL-316,243 led to decreased plasma levels of hemoglobin A1c, glucose, insulin, triglyceride and free fatty acid, and to an increased plasma adiponectin levels. It also improved insulin resistance in the oral glucose tolerance test. Adiponectin mRNA expression was significantly higher in the CL-316,243-treatment group than in the control group in epididymal white adipose tissue but not in brown adipose tissue, soleus muscle or liver. Adiponectin receptor 2 mRNA expression was significantly lower only in the liver of the CL-316,243-treatment group (versus the control group). These results suggest that the increased plasma adiponectin levels seen in db/db mice treated with this beta3-adrenoceptor agonist induce a down-regulation of adiponectin receptor 2 mRNA expression specifically in the liver.

Adiponectin↗
PubMed2005

Serum adiponectin correlates with viral characteristics but not histologic features in patients with chronic hepatitis C.

BACKGROUND/AIMS: Adiponectin induces insulin sensitivity and modulates inflammatory responses. We thus studied the implications of adiponectin in patients with chronic hepatitis C virus (HCV) infection inherently linked to insulin resistance. METHODS: We analyzed the association of serum adiponectin levels with clinical, virologic, and histologic findings in 95 naive Taiwanese patients with chronic hepatitis C before and after antiviral therapy. RESULTS: At baseline, 14 (15%) of the 95 patients were obese and 26 (27%) had type 2 diabetes mellitus. Fifty-seven patients were infected with HCV genotype 1 and 38 with genotype 2. Steatosis and periportal fibrosis was present in 44 (46%) and 69 (73%), respectively. In multivariate analysis, male gender, insulin resistance, high HCV load and genotype 2 were significantly associated with a lower serum adiponectin level. In contrast, intrahepatic gene expression of adiponectin receptors was higher in genotype 2 compared with genotype 1. Serum adiponectin level did not correlate with other clinical or histologic parameters. After treatment, change of steatosis also did not correlate with the change of adiponectin level (P=0.61). CONCLUSIONS: Adiponectin correlated with hepatitis C viral factors at both serum and liver tissue levels. The interactions among adiponectin, insulin resistance and chronic HCV infection merit further studies.

Adiponectin↗
PubMed2006

Angiotensin II infusion decreases plasma adiponectin level via its type 1 receptor in rats: an implication for hypertension-related insulin resistance.

We explored the mechanisms underlying the close association between hypertension and insulin resistance by measuring the changes in the plasma levels of adiponectin, a novel insulin sensitizer secreted by adipose tissue, in rats infused with angiotensin II (AII). Angiotensin II (100 ng/kg per minute) was subcutaneously infused with osmotic minipumps for 2 weeks in rats fed with either standard chow or a high-fructose diet. Insulin sensitivity index (SI) was assessed by the minimal model of Bergman [Diabetes 1989;38:1512-27]. Angiotensin II infusion significantly increased blood pressure and decreased SI. Angiotensin II decreased plasma adiponectin levels from 3.7 to 2.9 microg/mL (P < .01) without affecting the expression of adiponectin messenger RNA in adipose tissue. Angiotensin II infusion did not affect plasma leptin and tumor necrosis factor alpha levels. An AII type 1 receptor blocker, olmesartan, restored the low adiponectinemia induced by the AII infusion (50 ng/kg per minute). Plasma adiponectin levels were significantly lower in fructose-fed rats (2.3 microg/mL) than in chow-fed rats. Angiotensin II induced no further decrease of adiponectin, whereas olmesartan increased adiponectin remarkably both with and without AII infusion. The AII type 2 receptor blocker PD123319 left the AII-induced hypoadiponectinemia unchanged in both chow- and fructose-fed rats. The AII type 2 receptor agonist CGP42112A also left the adiponectin unchanged. Plasma adiponectin levels were substantially correlated with SI (r = 0.61, P < .0001). These results suggest that AII suppresses adiponectin production via AII type 1 receptor, resulting in impaired insulin sensitivity.

Adiponectin↗
PubMed2003

Cloning of adiponectin receptors that mediate antidiabetic metabolic effects.

Adiponectin (also known as 30-kDa adipocyte complement-related protein; Acrp30) is a hormone secreted by adipocytes that acts as an antidiabetic and anti-atherogenic adipokine. Levels of adiponectin in the blood are decreased under conditions of obesity, insulin resistance and type 2 diabetes. Administration of adiponectin causes glucose-lowering effects and ameliorates insulin resistance in mice. Conversely, adiponectin-deficient mice exhibit insulin resistance and diabetes. This insulin-sensitizing effect of adiponectin seems to be mediated by an increase in fatty-acid oxidation through activation of AMP kinase and PPAR-alpha. Here we report the cloning of complementary DNAs encoding adiponectin receptors 1 and 2 (AdipoR1 and AdipoR2) by expression cloning. AdipoR1 is abundantly expressed in skeletal muscle, whereas AdipoR2 is predominantly expressed in the liver. These two adiponectin receptors are predicted to contain seven transmembrane domains, but to be structurally and functionally distinct from G-protein-coupled receptors. Expression of AdipoR1/R2 or suppression of AdipoR1/R2 expression by small-interfering RNA supports our conclusion that they serve as receptors for globular and full-length adiponectin, and that they mediate increased AMP kinase and PPAR-alpha ligand activities, as well as fatty-acid oxidation and glucose uptake by adiponectin.

Adiponectin↗
PubMed2006

Regulation of adiponectin and its receptors in response to development of diet-induced obesity in mice.

Adiponectin and its receptors play an important role in energy homeostasis and insulin resistance, but their regulation remains to be fully elucidated. We hypothesized that high-fat diet would decrease adiponectin but increase adiponectin receptor (AdipoR1 and AdipoR2) expression in diet-induced obesity (DIO)-prone C57BL/6J and DIO-resistant A/J mice. We found that circulating adiponectin and adiponectin expression in white adipose tissue are higher at baseline in C57BL/6J mice compared with A/J mice. Circulating adiponectin increases at 10 wk but decreases at 18 wk in response to advancing age and high-fat feeding. However, adiponectin levels corrected for visceral fat mass and adiponectin mRNA expression in WAT are affected by high-fat feeding only, with both being decreased after 10 wk in C57BL/6J mice. Muscle AdipoR1 expression in both C57BL/6J and A/J mice and liver adipoR1 expression in C57BL/6J mice increase at 18 wk of age. High-fat feeding increases both AdipoR1 and AdipoR2 expression in liver in both strains of mice and increases muscle AdipoR1 expression in C57BL/6J mice after 18 wk. Thus advanced age and high-fat feeding, both of which are factors that predispose humans to obesity and insulin resistance, are associated with decreasing adiponectin and increasing AdipoR1 and/or AdipoR2 levels.

Adiponectin↗
PubMed2006

Adiponectin normalizes LPS-stimulated TNF-alpha production by rat Kupffer cells after chronic ethanol feeding.

Chronic ethanol feeding sensitizes Kupffer cells to activation by lipopolysaccharide (LPS), leading to increased production of tumor necrosis factor-alpha (TNF-alpha). Adiponectin treatment protects mice from ethanol-induced liver injury. Because adiponectin has anti-inflammatory effects on macrophages, we hypothesized that adiponectin would normalize chronic ethanol-induced sensitization of Kupffer cells to LPS-mediated signals. Serum adiponectin concentrations were decreased by 45% in rats fed an ethanol-containing diet for 4 wk compared with pair-fed rats. Adiponectin dose dependently inhibited LPS-stimulated accumulation of TNF-alpha mRNA and peptide in Kupffer cells from both pair- and ethanol-fed rats. Kupffer cells from ethanol-fed rats were more sensitive to both globular (gAcrp) and full-length adiponectin (flAcrp) than Kupffer cells from pair-fed controls with suppression at 10 ng/ml adiponectin after chronic ethanol feeding. Kupffer cells expressed both adiponectin receptors 1 and 2; chronic ethanol feeding did not change the expression of adiponectin receptor mRNA or protein. gAcrp suppressed LPS-stimulated ERK1/2 and p38 phosphorylation as well as IkappaB degradation at 100-1,000 ng/ml in Kupffer cells from both pair- and ethanol-fed rats. However, only LPS-stimulated ERK1/2 phosphorylation was sensitive to 10 ng/ml gAcrp. gAcrp also normalized LPS-stimulated DNA binding activity of early growth response-1 with greater sensitivity in Kupffer cells from rats fed chronic ethanol. In conclusion, these results demonstrate that Kupffer cells from ethanol-fed rats are more sensitive to the anti-inflammatory effects of both gAcrp and flAcrp. Suppression of LPS-stimulated ERK1/2 signaling by low concentrations of gAcrp was associated with normalization of TNF-alpha production by Kupffer cells after chronic ethanol exposure.

Adiponectin↗
PubMed2006

Adiponectin does not cross the blood-brain barrier but modifies cytokine expression of brain endothelial cells.

Adiponectin has recently been reported to generate a negative energy balance by increasing energy expenditure. However, it is unclear whether such effects require the presence and direct action of the adiponectin protein in the central nervous system. In this study, neither radiolabeled nonglycosylated nor glycosylated globular adiponectin crossed the blood-brain barrier (BBB) in mice. In addition, adiponectin was not detectable in human cerebrospinal fluid using various established methods. Using murine cerebral microvessels, we demonstrated expression of adiponectin receptors, which are upregulated during fasting, in brain endothelium. Interestingly, treatment with adiponectin reduced secretion of the centrally active interleukin-6 from brain endothelial cells, a phenomenon that was paralleled by a similar trend of other proinflammatory cytokines. In summary, our data suggest that direct effects of endogenous adiponectin on central nervous system pathways are unlikely to exist. However, the identification of adiponectin receptors on brain endothelial cells and the finding of a modified secretion pattern of centrally active substances from BBB cells provides an alternate explanation as to how adiponectin may evoke effects on energy metabolism.

Adiponectin↗
PubMed2004

Changes in adipocyte hormones leptin, resistin, and adiponectin in thyroid dysfunction.

Thyroid hormones as well as the recently discovered secretory products of adipose tissue adiponectin and resistin take part in energy metabolism. To study the changes in the adipocyte hormones with changes in the thyroid functional status, we measured adiponectin, resistin, and leptin in 69 subjects with Graves' disease before and 32 patients at follow up after treatment for hyperthyroidism at hypothyroid state. Concentrations of serum adiponectin and resistin were higher in hyperthyroid state than in hypothyroid state (adiponectin: 5.73 +/- 1.1 vs. 3.0 +/- 0.5 ng/ml, P = 0.03) (resistin: 6.378 +/- 0.6 vs. 5.81 +/- 0.57 ng/ml, P < 0.0001). Resistin levels correlate positively with free t4(r = 0.37, P < 0.01), free t3 levels(r = 0.33, P < 0.01) and negatively with TSH(r = -0.22, P < 0.05). Adiponectin levels correlate with free t4(r = 0.33, P < 0.01) and free t3 (r = 0.44, P < 0.01). Though the adiponectin levels did not correlate with leptin or resistin levels, strong positive correlation of both resistin and adiponectin with thyroid hormones is noted. Serum levels of leptin did not change with change in the thyroid functional status (leptin: 53.38 +/- 2.47 vs. 55.10 +/- 2.58 NS). Leptin levels did not correlate with resistin and adiponectin. We conclude that thyroid function has effect on adipocyte hormones adiponectin and resistin but not leptin.

Adipocytes↗