Increased Adiponectin Levels Research Articles

The leptin to adiponectin ratio (LAR) is reduced by sleeve gastrectomy in adults with severe obesity: a prospective cohort study

Bariatric surgery is known to reduce leptin and increase adiponectin levels, but the influence of sleeve gastrectomy on the leptin: adiponectin ratio (LAR), a measure of insulin sensitivity and cardiovascular risk, has not previously been described. We sought to determine the influence of sleeve gastrectomy on LAR in adults with severe obesity.In a single centre prospective cohort study of adults undergoing laparoscopic sleeve gastrectomy over a four-month period in our unit, we measured LAR preoperatively and 12 months after surgery. Of 22 patients undergoing sleeve gastrectomy, 17 (12 females, 12 with type 2 diabetes) had follow-up LAR measured at 12.1 ± 1 months. Mean body weight decreased from 130.6 ± 30.8 kg to 97.6 ± 21.6 kg, body mass index (BMI) from 46.9 ± 7.8 to 35.3 ± 7.2 kg m−2 and excess body weight from 87.5 ± 31.3 to 41.3 ± 28.8% (all p < 0.001). The reduction in leptin from 40.7 ± 24.9 to 30.9 ± 30.5 ng/ml was not significant (p = 0.11), but adiponectin increased from 4.49 ± 1.6 to 8.93 ± 6.36 µg/ml (p = 0.005) and LAR decreased from 8.89 ± 4.8 to 5.26 ± 6.52 ng/µg (p = 0.001), equivalent to a 70.9% increase in insulin sensitivity. The correlation with the amount of weight lost was stronger for LAR than it was for leptin or adiponectin alone. In this single-centre, interventional prospective cohort, patients undergoing laparoscopic sleeve gastrectomy had a substantial reduction in their LAR after 12 months which was proportional to the amount of weight lost. This may indicate an improvement in insulin sensitivity and a reduction in cardiovascular risk.

Metabolic cardio- and reno-protective effects of empagliflozin in a prediabetic rat model.

The mechanisms behind the cardiovascular and renal benefits of empagliflozin is not fully understood. The positive impact of the medication on cardiovascular mortality can not be solely attributed to its antidiabetic effect, with a metabolic mechanism possibly involved. To investigate the metabolic effects of empagliflozin treatment (10 mg/kg/day for 6 weeks), we used an adult male rat model with serious vascular complications associated with metabolic syndrome and prediabetes. Impaired glucose tolerance, severe albuminuria and impaired insulin sensitivity were induced by intragastric administration of methylglyoxal and high sucrose diet feeding for four months. Although empagliflozin decreased body weight, non-fasting glucose and insulin, glucagon levels remained unchanged. In addition, empagliflozin increased adiponectin levels (+40%; p < 0.01) and improved skeletal muscle insulin sensitivity. Increased non-esterified fatty acids (NEFA) in empagliflozin-treated rats is understood to generate ketone bodies. Empagliflozin increased β-hydroxybutyrate levels in serum (+66%; p < 0.05) and the myocardium (30%; p < 0.01), suggesting its possible involvement as an alternative substrate for metabolism. Empagliflozin switched substrate utilisation in the myocardium, diverting glucose oxidation to fatty acid oxidation. Representing another favorable effect, empagliflozin also contributed to decreased uric acid plasma levels (-19%; p < 0.05). In the kidney cortex, empagliflozin improved oxidative and dicarbonyl stress parameters and increased gene expression of β-hydroxybutyrate dehydrogenase, an enzyme involved in ketone body utilisation. In addition, empagliflozin decreased microalbuminuria (-27%; p < 0.01) and urinary neutrophil gelatinase-associated lipocalin (NGAL) excretion (-29%; p < 0.01). Our results reveal the important systemic metabolic effect of empagliflozin on alterations in substrate utilisation and on increased ketone body use in prediabetic rats. Improved oxidative and dicarbonyl stress and decreased uric acid are also possibly involved in the cardio- and reno-protective effects of empagliflozin.

Activation of AT2 receptors prevents diabetic complications in female db/db mice by NO-mediated mechanisms.

The AT2 receptor plays a role in metabolism by opposing the actions triggered by the AT1 receptors. Activation of AT2 receptors has been shown to enhance insulin sensitivity in both normal and insulin resistance animal models. In this study, we investigated the mechanism by which AT2 receptors activation improves metabolism in diabetic mice. Female diabetic (db/db) and non-diabetic (db/+) mice were treated for 1 month with the selective AT2 agonist, compound 21 (C21, 0.3 mg·kg-1 ·day-1 , s.c.). To evaluate whether the effects of C21 depend on NO production, a subgroup of mice was treated with C21 plus a sub-pressor dose of the NOS inhibitor l-NAME (0.1 mg·ml-1 , drinking water). C21-treated db/db mice displayed improved glucose and pyruvate tolerance compared with saline-treated db/db mice. Also, C21-treated db/db mice showed reduced liver weight and decreased hepatic lipid accumulation compared with saline-treated db/db mice. Insulin signalling analysis showed increased phosphorylation of the insulin receptor, Akt and FOXO1 in the livers of C21-treated db/db mice compared with saline-treated counterparts. These findings were associated with increased adiponectin levels in plasma and adipose tissue and reduced adipocyte size in inguinal fat. The beneficial effects of AT2 receptors activation were associated with increased eNOS phosphorylation and higher levels of NO metabolites and were abolished by l-NAME. Chronic C21 infusion exerts beneficial metabolic effects in female diabetic db/db mice, alleviating type 2 diabetes complications, through a mechanism that involves NO production.

Role of Exercise-induced Adiponectin Activation on Obese and Diabetic Individuals

PURPOSE: The physiological role of adipocytokines on obesity, diabetes, and insulin resistance is not clearly understood yet. Furthermore, the mechanism of exercise-induced changes in plasma adiponectin in obesity and diabetes is not known well. The aim of this review is to describe the role of exercise on the adiponectin production in adipose tissue of the obesity and diabetes.METHODS: This study reviews 46 previous studies focusing on the effect of exercise on adiponectin in obese and diabetic individuals.RESULTS: Increasing adiponectin levels after long-term exercise training in obese and diabetic individuals have inconsistent support in the scientific literature. However, the present review summarized evidence that supports for exercise training as a viable strategy to increase adiponectin in obese and diabetic individuals.CONCLUSIONS: Despite the importance of regular physical activity for the prevention of obesity and diabetes outlined in numerous guidelines and recommendations, previous studies showed inconsistent results regarding the effect of physical activity among obese and diabetic individuals. This review suggested that exercise training induces the augmentation of the anti-inflammatory cytokine adiponectin and in turn, it provides long-term health outcomes for obese and diabetic individuals.

Influence of n-3 fatty acid supplementation on inflammatory and oxidative stress markers in patients with polycystic ovary syndrome: a systematic review and meta-analysis

Polycystic ovary syndrome (PCOS) is defined as a reproductive endocrine disease that results in a low-grade inflammatory and pro-oxidant state. Dietary factors, including n-3 fatty acids, may have a key role in improving metabolic disorders in PCOS patients. The present study aimed to investigate the influence of n-3 fatty acid supplementation on inflammatory and oxidative stress (OS) markers in patients with PCOS. A systematic literature search of Medline/PubMed, Cochrane Central Register of Controlled Trials, Scopus and Lilacs, until November 2019, was conducted. Randomised clinical trials that reported inflammatory and OS markers as endpoints in women with PCOS receiving n-3 fatty acid supplementation were included. The pooled estimates of the weighted mean differences (WMD) and the standard mean differences (SMD) were calculated. Random effects models were adopted to measure the pooled outcomes. Among the 323 studies retrieved, ten fulfilled the inclusion criteria for a meta-analysis. We founded a significant decrease in high-sensitivity C-reactive protein (hs-CRP) (SMD -0·29 (95 % CI -0·56, -0·02) mg/l) and an increase in adiponectin (WMD 1·42 (95 % CI 1·09, 1·76) ng/ml) concentrations in the intervention group when compared with the placebo group. No statistically significant results were found in the meta-analysis for visfatin, nitric oxide, GSH or malondialdehyde levels or total antioxidant capacity. The data suggest that supplementation of n-3 fatty acids could reduce the inflammatory state in women with PCOS, through a decrease in hs-CRP and an increase in adiponectin levels.

Azilsartan medoxomil for improving insulin resistance and adipokine levels in hypertension in comparison with angiotensin-converting enzyme inhibitors

Aim. To assess azilsartan medoxomil (AZM) in achieving the target blood pressure (BP) (<140/90 mm Hg), its angioprotective action in patients with hypertension (HTN), as well as contribution in reducing levels of adipokines and inflammation markers in patients switching from lisinopril or enalapril. Material and methods. This open-label observational study lasting 24 weeks included 60 patients who had previously received monotherapy with lisinopril 20 mg/day or enalapril 20 mg/day, and did not reach the target BP levels (<140/90 mm Hg). During the study, all patients underwent 24-hour BP monitoring, applanation tonometry (determination of the augmentation index and central BP), pulse wave velocity measurement, laboratory tests (lipid profile, uric acid, fasting glucose, HOMA index, homocysteine, leptin, adiponectin, highly sensitive C-reactive protein (hs-CRP), tumor necrosis factor alpha, interleukin-6 (IL-6). Results. After switching from lisinopril and enalapril to AZM, a decrease in systolic BP was 24,3% and 31,3%, diastolic BP — 19,8% and 21,4% (p<0,05). In the groups of initial therapy with lisinopril and enalapril, there was a decrease in central (aortic) BP by 20,4% and 25,5%, central pulse pressure by 20,6% and 27,6%, augmentation index by 33,1% and 34,58%, pulse wave velocity by 19,4% and 20,7% (p<0,05), levels of leptin by 10,4%, and 16,8%, hs-CRP by 16,1% and 19,3%, IL-6 by 23,6% and 25,1%, respectively. We also revealed an increase in adiponectin levels by 7,2% and 9,2%, respectively (p<0,05). Conclusion. Azilsartan medoxomil has advantages over angiotensin-converting enzyme inhibitors (enalapril, lisinopril) in achieving BP control, and improving vascular elasticity. It contributes to a decrease in insulin resistance and noninfectious inflammation.

The Effect of Training (Aerobic and Concurrent) and Cinnamon Supplementation on the Plasma Levels of Visfatin and Adiponectin in Overweight Diabetic Men

Background: Diabetes is one of the most prevalent diseases caused by metabolic disorders, which is considered as a major global challenge. Objectives: The aim of this study was to compare the effects of two aerobic and concurrent (aerobic and resistance training) training protocols with supplementation of cinnamon on the level of some selected adipokines (visfatin and adiponectin) in overweight men with type 2 diabetes. Methods: for this purpose among The overweight and type II diabetic men in Kermanshah who were referred to a medical clinic, fifty people with BMI 28.55 ± 2.52 and age of 45.98 ± 6.79 who were volunteer to participate in research design, divided in five 10 people group consist of four experimental and one control group randomly. The experimental groups involve aerobic training, concurrent training, aerobic training along with cinnamon supplementation and eventually concurrent training along with cinnamon supplementation. While the experimental groups did the specific training, the control groups did no training throughout research design. Blood sampling were taken in experimental and control groups during pretest and posttest from anterior brachial vein. The variables were measured by ELISA method. Results: The results of ANCOVA and Bonferroni tests showed that both aerobic training and concurrent training (aerobic and resistance training) with and without cinnamon supplementation caused significant increase in plasma levels of adiponectin and significant decrease in plasma levels of visfatin in type two diabetic men.8 weeks of concurrent training in comparing with aerobic training was more effective in increasing the plasma levels of adiponectin and the difference between them was significant but the difference about plasma level of visfatin was insignificant. Conclusions: The results of this study showed that the effect of both aerobic and concurrent training with and without cinnamon supplementation has significant effect on plasma levels of adiponectin and visfatin and except more increase in adiponectin level in concurrent group in comparing with aerobic group, nearly there are no differences in terms of training type and taking and no taking of cinnamon supplementation. Based the finding of this study, both aerobic and concurrent training especially with cinnamon supplementation is effective in improving the health of men with type 2 and overweight diabetes.

Caffeine Upregulates Hepatic Sex Hormone-Binding Globulin Production by Increasing Adiponectin Through AKT/FOXO1 Pathway in White Adipose Tissue.

Epidemiological studies have shown that caffeine increases serum sex hormone-binding globulin (SHBG) levels. The relationship between caffeine and SHBG production has never been studied before at molecular level. The aim of this study is to examine whether caffeine regulates SHBG production and to determine the associated molecular mechanisms. Two different studies are performed; in vitro studies using human HepG2 cells treated with caffeine (100 and 500 µm) and in vivo studies using a humanized SHBG transgenic mice drinking caffeine in the water (0.1 mg mL-1 ) for 12 days. The results show that caffeine does not change SHBG production in HepG2 cells. By contrast, caffeine treatment increases significantly hepatic SHBG production in human SHBG transgenic mice when compared with control mice. Caffeine increases adiponectin levels in epididymal adipose tissue of human SHBG transgenic mice. Moreover, caffeine increases adiponectin production by reducing protein kinase B (AKT) phosphorylation which increases forkhead box protein O1 (FOXO1) protein levels in 3T3-L1 mature adipocytes and human SHBG transgenic mice. Finally, caffeine-induced increase in adiponectin in turn upregulates hepatic hepatocyte nuclear receptor 4-alpha (HNF-4α) levels in human SHBG transgenic mice. The results show that caffeine upregulates hepatic SHBG expression by increasing adiponectin production through AKT/FOXO1 pathway in the adipose tissue.

The effect of evening primrose oil (Oenothera biennis) on the level of adiponectin and some biochemical parameters in rats with fructose induced metabolic syndrome

The effect of evening primrose oil on adiponectin level and some biochemical parameters in model of fructose-induced metabolic syndrome were investigated. The rats were divided into 4 groups: control, evening primrose oil, fructose, fructose + evening primrose oil. Body weight, daily feed and water consumptions and systolic blood pressures of animals were measured. At the end of trial, blood samples were taken, livers were excised and histopathological examination was performed. Glucose, uric acid, triglyceride, T.cholesterol, LDL, HDL, VLDL, ALT, AST, ALP, LDH, adiponectin, insulin, IL-6, TNF-α, TAC, and TOS levels were analysed. Some analysed parameters and systolic blood pressure of fructose + evening primrose oil group decreased significantly compared to fructose group and adiponectin, TAC, and HDL levels were significantly increased. As conclusion, evening primrose oil can be considered as antioxidant agent by reducing oxidative stress, increasing adiponectin levels and insulin sensitivity, anti-inflammatory properties, exhibiting anti-atherogenic effect by regulating dyslipidemia and systolic blood pressure.

Orlistat attenuates obesity‐induced decline in steroidogenesis and spermatogenesis by up‐regulating steroidogenic genes

Steroidogenesis decline is reported to be one of the mechanisms associated with obesity-induced male factor subfertility/infertility. We explored the possible preventive/therapeutic effects of orlistat (a medication prescribed for weight loss) on obesity-induced steroidogenesis and spermatogenesis decline. Twenty-four adult male Sprague Dawley rats weighing 250-300g were randomized into four groups (n=6/group), namely; normal control, high-fat diet, high-fat diet plus orlistat preventive group and high-fat diet plus orlistat treatment group. Orlistat (10mg/kg/b.w./d suspended in distilled water) was either concurrently administered with high-fat diet for 12weeks (high-fat diet plus orlistat preventive group) or administered from week 7-12 post- high-fat diet feeding (high-fat diet plus orlistat treatment group). Thereafter, serum, testes and epididymis were collected for analyses. Obesity increased serum leptin and decreased adiponectin levels, decreased serum and intra-testicular levels of follicle stimulating hormone, luteinising hormone and testosterone, sperm count, motility, viability, normal morphology and epididymal antioxidants, but increased epididymal malondialdehyde level and sperm nDNA fragmentation. Testicular mRNA transcript levels of androgen receptor, luteinizing hormone receptor, steroidogenic acute regulatory protein, cytochrome P450 enzyme (CYP11A1), 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase were significantly decreased in the testes of the high-fat diet group. Further, the levels of steroidogenic acute regulatory protein protein and enzymatic activities of CYP11A1, 3β-hydroxysteroid dehydrogenase and 17β-hydroxysteroid dehydrogenase were also significantly decreased in the testes of the high-fat diet group. Treatment with orlistat significantly decreased leptin and increased adiponectin levels, improved sperm parameters, decreased sperm DNA fragmentation, increased the levels of steroidogenic hormones, proteins and associated genes in high-fat diet-induced obese male rats, with the preventive group (high-fat diet plus orlistat preventive group) having better results relative to the treatment group (high-fat diet plus orlistat treatment group). Orlistat attenuated impaired spermatogenesis and steroidogenesis decline by up-regulating steroidogenic genes. This may not be unconnected to its significant effect in lowering serum leptin levels, since the hormone is known to dampen fertility potential. Therefore, orlistat may improve fertility potential in overweight/obese men.

Lactobacillus M5 prevents osteoarthritis induced by a high-fat diet in mice

• M5 attenuated high-fat diet induced obesity through modification of mice gut microbiota. • M5 significantly reduced leptin levels and increased adiponectin levels, while decreased levels of TNF-α were observed, which would promote the prevention of OA. • M5 effectively inhibited the development of OA by reducing body weight, protecting cartilage from damage, regulating adipokines levels and gut microbiota composition in mice. A long-term high-fat diet (HFD) can cause OA through biomechanical and metabolic factors, which may be related to changes in the gut microbiota. The purpose of the present study was to evaluate the roles of L. paracasei subsp. paracasei M5 (M5) and CS in the prevention of OA caused by HFD and the relationship between the gut microbiota and OA. The results showed that mice receiving an HFD had significantly increased body weight and exhibited characteristics associated with OA. Both M5 and CS effectively prevented the destruction of articular cartilage and the degradation of type II collagen caused by HFD. The level of serum and infrapatellar fat pad (IPFP) leptin was also significantly decreased. A strong predictive relationship was observed between the abundance of Ruminococcaceae_UCG-014 , Streptococcus , Bacteroides and OA. In summary, we demonstrated that M5 protected against HFD-induced OA, which was probably associated with modification of the gut microbiota.

Naringin reduces body weight, plasma lipids and increases adiponectin levels in patients with dyslipidemia.

Naringin is a citrus-flavonoid which has been shown to have positive metabolic and anti-inflammatory effects. For this reason, we believe it would be interesting to study the effects of Naringin administration on body weight, BMI, lipid profile and adiponectin levels in patients with dyslipidemia, especially considering that dyslipidemias along with obesity and subsequent cardiometabolic complications are some of the most important public health issues plaguing our society today. A double-blind, randomized clinical trial was conducted in a group of 28 adult patients previously diagnosed with dyslipidemia who attended the Institute of Experimental and Clinical Therapeutics. Patients were divided into two groups; the first group (n=14) received 450mg of naringin every 24hours, in the mornings, while the second group (n=14) was given a homologated placebo over the course of a 90-day period. Significant differences were observed in naringin group compared to the placebo group in terms of decreased BMI (30.6±3.19 vs 33.3±3.23kg/m2; p=0.03), total cholesterol (182±20.2 vs 245±24.1mg/dl; p<0.01), LDL cholesterol (100±17.5 vs 125±38.3mg/dl; p=0.03) and an increase in adiponectin levels (0.82±0.25 vs 0.59±0.19μg/ml; p=0.01). Our results support the use of Naringin as a potential therapeutic agent which could play an important role in the management of metabolic disorders.

1709-P: Increased Adiponectin Levels Are Associated with Impaired Brown Adipose Tissue in Mice

Brown adipose tissue (BAT) thermogenesis affects energy expenditure, as well as glucose and lipid clearance. Thus, making BAT an attractive target in obesity/type-2 diabetes. Adiponectin (Apn) regulates whole-body metabolism and lowered Apn levels are associated with obesity and increased type-2 diabetes risk. Apn has been suggested to be required for maintaining normal body temperature in cold environment, but the role of Apn in BAT functionality is not clear. Here, we have studied BAT in adiponectin overexpressing (Apn-Tg) mice. During unchallenged chow-diet conditions, BAT of Apn-Tg mice was enlarged, fibrotic and more whitish. This phenotype was, as judged by tracer experiments, associated with lower lipid and glucose uptake, decreased de novo lipogenesis and decreased fatty acid oxidation in BAT. High-fat diet (HFD)-induced obesity increased these differences between genotypes. The BAT mRNA expression of thermogenesis markers such as UCP-1 and DIO-2 were down-regulated in BAT of obese, but not lean, Apn-Tg mice. Moreover, Seahorse-based analysis revealed reduced mitochondrial function in Apn-Tg BAT in ex vivo-differentiated brown adipocytes. To test whether increased Apn levels affect cold-induced BAT activation, we exposed Apn-tg and littermate control mice to cold temperature (6°C) for four weeks. Under this setting, the BAT lipid and glucose uptake, and body temperature were similar between genotypes. Accordingly, UCP-1 and DIO-2 mRNA levels were not different between Apn-Tg and WT mice, and highly induced by chronic cold exposure. Nevertheless, Seahorse data from isolated BAT mitochondria from cold-exposed animals still indicate mitochondrial dysfunction in Apn-Tg mice. Thus, our data suggest that increased adiponectin levels are associated with metabolic dysfunction in BAT. We propose that the increased BAT expansion in Apn-Tg mice occurs at the expense of the mitochondrial function. Disclosure B. Chanclon: None. M. Bauza-Thorbrugge: None. A. Benrick: None. I. Wernstedt-Asterholm: None.

Effect of two different dietary fatty acid profiles and variant rs266729 in ADIPOQ on weight loss and adiponectin concentrations

BackgroundThe role of ADIPOQ gene rs266729 variants on weight loss after a dietary intervention are still unclear. ObjectiveTo analyze the effects of the ADIPOQ gene rs266729 variant n weight loss, cardiovascular risk factors, and adiponectin levels after two hypocaloric diets with different dietary fatty profiles. DesignA population of 362 obese patients was enrolled in a randomized clinical trial with two diets (Diet M, monounsaturated fat-enriched diet, and Diet P, polyunsaturated-fat enriched diet). Anthropometric measurements, an assessment of nutritional intake, and biochemical tests were performed at baseline and after 12 weeks. ResultsWeight loss was similar with both diets. After Diet M, only subjects with CC genotype showed significant improvements in total cholesterol (CC vs. CG±GG) (−9.0±1.1mU/L vs. −4.5±2.4mg/dL, p=0.01), LDL cholesterol (−6.0±1.1mg/dL vs. −3.0±0.9mg/dL, p=0.03), glucose (−4.7±1.1mg/dL vs. −0.6±0.5mg/dL, p=0.01), and insulin levels (−2.6±1.0mU/L vs. −0.7±0.3mU/L, p=0.02) and in HOMA-IR (−0.5±0.2 units vs. −0.2±0.4 units, p=0.03). The same improvement was reported after Diet P in all parameters, including total cholesterol (CC vs. CG±GG) (−8.0±1.2mU/L vs. −2.1±1.4mg/dL, p=0.02), LDL cholesterol (−7.3±1.2mg/dL vs. −2.1±0.8mg/dL, p=0.02), glucose (−3.2±0.1mg/dL vs. −0.2±0.5mg/dL, p=0.01), and insulin levels (−2.5±1.0mU/L vs. −1±0.6mU/L, p=0.02) and HOMA-IR (−0.5±0.1 units vs. −0.3±0.4 units, p=0.02). Only subjects with CC genotype showed significant increases in adiponectin levels after both diets: (Diet M: 10.3±2.0ng/dL vs. Diet P: 9.3±2.9ng/dL, p=0.43). ConclusionThe CC genotype of ADIPOQ gene rs266729 variant is associated to increased adiponectin levels and decreases in LDL cholesterol, glucose, insulin, and HOMA-IR levels after weight loss.

Metabolic Syndrome, Disease Activity, and Adipokines in Patients With Newly Diagnosed Inflammatory Joint Diseases.

To investigate metabolic syndrome (MetS), disease activity, and adipokine levels among patients with rheumatoid arthritis (RA), spondyloarthritis (SpA), and undifferentiated arthritis (UA) at the time of diagnosis and after 1 year of follow-up. Patients with inflammatory joint diseases participating in the Northern Savo 2010 population-based longitudinal epidemiological study were evaluated for components of MetS (by National Cholesterol Education Program's Adult Treatment Panel III) and clinical parameters of disease activity. The adipokines adiponectin, adipsin, resistin, and leptin were measured at baseline and after 1 year of treatment with disease-modifying antirheumatic drugs. Among 176 patients, MetS was detected in 42% of RA, 36% of SpA, and 51% of UA patients. Metabolic syndrome was associated with higher disease activity as measured by patient global assessment in RA and UA patients and increased pain in RA patients. Leptin levels were increased in patients with MetS, showing a linearly increasing trend with the number of components of MetS in SpA and UA, but not in RA. In RA patients, decrease in disease activity correlated with decrease in leptin levels. Resistin did not associate with MetS, but a decrease in resistin correlated with decrease in disease activity in RA and UA. In SpA, increased adiponectin level correlated with relief in disease activity, but not with MetS. Metabolic syndrome was common in patients with newly diagnosed arthritides and associated with higher disease activity and increased leptin levels. Resistin responded to treatment of arthritis in RA and UA, leptin in RA, and adiponectin in SpA.

Dietary Melatonin Protects Against Behavioural, Metabolic, Oxidative, and Organ Morphological Changes in Mice that are Fed High-Fat, High- Sugar Diet.

Metabolic syndrome is a complex pattern of disorders that occur jointly and is associated with an increased risk of cardiovascular and cerebrovascular disease. Therefore the need for more-efficient options of treatment has become imperative. This study examined the effect of dietary-melatonin in the management of behavioural, metabolic, antioxidant, and organ changes due to high-fat/high-sugar (HFHS) diet-induced metabolic syndrome in mice. Mice were randomly assigned into five groups of ten animals each. Groups were normal control [fed standard diet (SD)], HFHS control, and 3 groups of melatonin incorporated into HFHS at 2.5, 5, and 10 mg/kg of feed. Mice were fed for seven weeks, and body weight was assessed weekly. Open-field behaviours, radial-arm, and Y-maze spatial memory were scored at the end of the experimental period. Twenty-four hours after the last behavioural test, blood was taken for estimation of blood glucose levels after an overnight fast. Animals were then euthanised, and blood was taken for estimation of plasma insulin, leptin, and adiponectin levels, and serum lipid profile. The liver, kidneys, and brain were excised and processed for general histology, while homogenates of the liver and whole brain were used to assess oxidative stress parameters. Results showed that dietary melatonin (compared to HFHS diet) was associated with a decrease in body weight, food intake, and novelty-induced behaviours; and an increase in spatial-working memory scores. A decrease in glucose, insulin, leptin, and malondialdehyde levels; and an increase in adiponectin levels and superoxide dismutase activity were also observed. Histomorphological/ histomorphometric examination revealed evidence of organ injury with HFHS diet, and varying degrees of amelioration with melatonin-supplemented diet. In conclusion, dietary melatonin supplementation may have beneficial effects in the management of the metabolic syndrome.

The Protective Effects of Acer okamotoanum and Isoquercitrin on Obesity and Amyloidosis in a Mouse Model.

Obesity increases risk of Alzheimer’s Disease (AD). A high fat diet (HFD) can lead to amyloidosis and amyloid beta (Aβ) accumulation, which are hallmarks of AD. In this study, protective effects of the ethyl acetate fraction of Acer okamotoanum (EAO) and isoquercitrin were evaluated on obesity and amyloidosis in the HFD- and Aβ-induced mouse model. To induce obesity and AD by HFD and Aβ, mice were provided with HFD for 10 weeks and were intracerebroventricularly injected with Aβ25–35. For four weeks, 100 and 10 mg/kg/day of EAO and isoquercitrin, respectively, were administered orally. Administration of EAO and isoquercitrin significantly decreased body weight in HFD and Aβ-injected mice. Additionally, EAO- and isoquercitrin-administered groups attenuated abnormal adipokines release via a decrease in leptin and an increase in adiponectin levels compared with the control group. Furthermore, HFD and Aβ-injected mice had damaged liver tissues, but EAO- and isoquercitrin-administered groups attenuated liver damage. Moreover, administration of EAO and isoquercitrin groups down-regulated amyloidosis-related proteins in the brain such as β-secretase, presenilin (PS)-1 and PS-2 compared with HFD and Aβ-injected mice. This study indicated that EAO and isoquercitrin attenuated HFD and Aβ-induced obesity and amyloidosis, suggesting that they could be effective in preventing and treating both obesity and AD.

Coenzyme Q10 Supplementation Improves Adipokine Levels and Alleviates Inflammation and Lipid Peroxidation in Conditions of Metabolic Syndrome: A Meta-Analysis of Randomized Controlled Trials.

Evidence from randomized controlled trials (RCTs) suggests that coenzyme Q10 (CoQ10) can regulate adipokine levels to impact inflammation and oxidative stress in conditions of metabolic syndrome. Here, prominent electronic databases such as MEDLINE, Cochrane Library, and EMBASE were searched for eligible RCTs reporting on any correlation between adipokine levels and modulation of inflammation and oxidative stress in individuals with metabolic syndrome taking CoQ10. The risk of bias was assessed using the modified Black and Downs checklist, while the Grading of Recommendations Assessment, Development and Evaluation (GRADE) tool was used to evaluate the quality of evidence. Results from the current meta-analysis, involving 318 participants, showed that CoQ10 supplementation in individuals with metabolic syndrome increased adiponectin levels when compared to those on placebo (SMD: 1.44 [95% CI: −0.13, 3.00]; I2 = 96%, p < 0.00001). Moreover, CoQ10 supplementation significantly lowered inflammation markers in individuals with metabolic syndrome in comparison to those on placebo (SMD: −0.31 [95% CI: −0.54, −0.08]; I2 = 51%, p = 0.07). Such benefits with CoQ10 supplementation were related to its ameliorative effects on lipid peroxidation by reducing malondialdehyde levels, concomitant to improving glucose control and liver function. The overall findings suggest that optimal regulation of adipokine function is crucial for the beneficial effects of CoQ10 in improving metabolic health.

Juzentaihoto extract suppresses adipocyte hypertrophy and improves hyperglycemia in KKAy mice.

Juzentaihoto is a herbal medicine with reported anti-inflammatory effects, and it is predicted to improve inflammation and insulin sensitivity within obesity. In the present study, juzentaihoto hot water extract (JTT) was administered to obese type 2 diabetic model mice (KKAy) for 56 days. In addition, the effects of JTT on the adipose tissue, glucose metabolism, and blood lipids were evaluated for examining its impact on insulin sensitivity and obesity. As a result of JTT administration, KKAy mice exhibited suppressed adipocyte hypertrophy, decreased the mRNA levels of tumor necrosis factor α, and increased the mRNA levels of adiponectin in epididymal fat tissue. In addition, fasting blood glucose levels, blood triglyceride, and total cholesterol decreased. In summary, these data indicated that JTT administration suppressed the production of inflammatory cytokines and increased adiponectin levels in the adipose tissue. Therefore, with improved insulin sensitivity, blood glucose, and lipid decreased.

Association of Adiponectin and IgE levels with occurrence of asthma in Babylon Province

ackground : Asthma is a health condition that affects breathing in people. Breathing comfortably is not something most of us need to think about. But if you have asthma, there are times when you have difficulty breathing.The main objectives in the current study are:Determine the role of adiponectin, a hormone that acts as an anti-inflammatory, In addition determine the concentration of immunoglobulin E (IgE) In asthma patients. Method: This study included two groups:Group 1: 80 Patients with asthma were divided into two parts (40 samples obese and 40 samples non-obese).Group 2: 80Group of healthy subjects with no history or clinical evidence of asthma. samples were divided into two parts (40 samples were obese and 40 were not obese). Asthma was diagnosed through a pulmonary function test (PFT) and then invited to a private clinic and measured nitric oxide gas (FeNO) to confirm the diagnosis.Enzyme-linked immunosorbent assay(ELISA ) technique was used to determine the concentration of adiponectin and IgE in serum. Results: The present study demonstrated the increase of adiponectin level with asthmatic patients compared with the control group and showed significant difference between non-obese patients group and non-obese healthy group. Conclusion: Adiponectin related with obesity play crucial role in asthma development and inverse relationship between IgE and adiponectin