Serum Levels of Resistin and Adiponectin in Women with Periodontitis: the Hisayama Study

Resistin and adiponectin, recently discovered adipokines, are secreted from adipose tissue, with postulated opposing functions in insulin resistance and inflammation. More recently, an abundance of resistin was detected in macrophages, which suggests its important role in inflammation. The aim of this study was to clarify circulating serum adipokine levels in women with periodontitis. Thirty-four women with moderate to severe periodontitis and 42 control individuals with healthy gingiva (50- to 59-year-old women) were selected. The serum level of adipokines was analyzed between groups, along with the obesity index, smoking status, and age. Having periodontitis was significantly associated with an increased level of resistin, both in bivariate (OR, 3.0; 95% CI, 1.2–7.6) and multivariate (adjusted OR, 3.1; 95% CI, 1.1–8.6) analyses. The association of periodontitis with a decreased level of adiponectin did not reach statistical significance. It was concluded that an increased serum resistin level in middle-aged Japanese women with periodontitis may affect systemic health.

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Plasma resistin, adiponectin and leptin levels in lean and obese subjects: correlations with insulin resistance

Acta Endocrinologica ◽

10.1530/eje.0.1490331 ◽

2003 ◽

Vol 149 (4) ◽

pp. 331-335 ◽

Cited By ~ 350

Author(s):

JV Silha ◽

M Krsek ◽

JV Skrha ◽

P Sucharda ◽

BL Nyomba ◽

...

Keyword(s):

Insulin Resistance ◽

Body Mass Index ◽

Adipose Tissue ◽

Statistical Significance ◽

Model Assessment ◽

Fasting Insulin ◽

Homeostasis Model Assessment ◽

Glucose Levels ◽

Obese Subjects ◽

The Relationship

OBJECTIVE: Adipose tIssue regulates insulin sensitivity via the circulating adipocytokines, leptin, resistin and adiponectin. The objective of this study was to compare the levels of resistin, adiponectin and leptin in lean and obese subjects and determine the relationship between circulating adipocytokines and insulin resistance. METHODS: We examined plasma levels of resistin, adiponectin and leptin in 17 lean subjects with a mean body mass index (BMI) of approximately 23 and 34 non-diabetic obese individuals with a mean BMI approximately 33. Insulin resistance was assessed using the homeostasis model assessment ratio (HOMA-R) formula derived from fasting insulin and glucose levels. RESULTS: Resistin levels were not significantly different between the two groups but were significantly higher in women compared with men, 35.4+/-6.5 (s.e.) vs 15.4+/-2.9 microg/L, P<0.01. Resistin did not correlate with BMI but did significantly correlate with HOMA-R, P<0.01, and this correlation remained significant after adjustment for gender and BMI. Adiponectin levels were significantly lower in obese compared with lean subjects, P<0.005, and higher in women, P<0.001, but showed no significant correlation with HOMA-R. Leptin levels were significantly higher in obese subjects and women and correlated with HOMA-R and resistin. DISCUSSION: In this small group of patients we demonstrated that insulin resistance correlated most strongly with leptin levels. A significant correlation between resistin levels and insulin resistance was also observed. Although a similar trend was apparent for adiponectin, the correlation with insulin resistance did not achieve statistical significance.

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Edible Red Seaweed Campylaephora Hypnaeoides J. Agardh Alleviates Obesity and Related Metabolic Disorders in Mice by Suppressing Oxidative Stress and Inflammatory Response

10.21203/rs.3.rs-877916/v1 ◽

2021 ◽

Author(s):

Shigeru Murakami ◽

Chihiro Hirazawa ◽

Rina Yoshikawa ◽

Toshiki Mizutani ◽

Takuma Ohya ◽

...

Keyword(s):

Insulin Resistance ◽

Adipose Tissue ◽

Hepatic Steatosis ◽

White Adipose Tissue ◽

Metabolic Disorders ◽

Public Health Problem ◽

Serum Levels ◽

Diet Group ◽

Raw264.7 Cells ◽

Edible Seaweed

Abstract Background: The obesity epidemic has become a serious public health problem in many countries worldwide. Seaweed has few calories and is rich in active nutritional components necessary for health promotion and disease prevention. The aim of this study was to investigate the effects of the Campylaephora hypnaeoides J. Agardh (C. hypnaeoides), an edible seaweed traditionally eaten in Japan, on high-fat (HF) diet-induced obesity and related metabolic diseases in mice.Methods: Male C57BL/6J mice were randomly divided into the following groups: normal diet group, HF diet group, HF diet supplemented with 2% C. hypnaeoides, and HF diet supplemented with 6% C. hypnaeoides. After 13 weeks of treatment, the weight of the white adipose tissue and liver, and the serum levels of glucose, insulin, adipokines, and lipids were measured. Hepatic levels of adipokines, oxidant markers, and antioxidant markers were also determined. Insulin resistance was assessed by a glucose tolerance test. Polysaccharides of C. hypnaeoides were purified and their molecular weight was determined by high-performance seize exclusion chromatography. The anti-inflammatory effects of purified polysaccharides were evaluated in RAW264.7 cells. Results: Treatment of HF diet-induced obese mice with C. hypnaeoides for 13 weeks suppressed the increase in body weight and white adipose tissue weight. It also ameliorated insulin resistance, diabetes, hepatic steatosis, and hypercholesterolemia. The ingestion of an HF diet increased serum levels of malondialdehyde (MDA), tumor necrosis factor a (TNF-a), and monocyte chemoattractant protein-1 (MCP-1), while it decreased serum adiponectin levels. In the liver, an HF diet markedly increased the MDA, TNF-a, and interleukin-6 (IL-6) levels, while it decreased glutathione (GSH) and superoxide dismutase (SOD). These metabolic changes induced by HF diet feeding were ameliorated by dietary C. hypnaeoides. Purified polysaccharides and ethanol extract from C. hypnaeoides inhibited the lipopolysaccharide-induced overproduction of nitric oxide and TNF-a in macrophage RAW264.7 cells. Conclusions: The present results indicated that C. hypnaeoides was able to alleviate HF diet-induced metabolic disorders, including obesity, diabetes, hepatic steatosis, and hypercholesterolemia by attenuating inflammation and improving the antioxidant capacity in mice. Polysaccharides and polyphenols may be involved in these beneficial effects of C. hypnaeoides.

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Insulin resistance and lung function in obese asthmatic pre-pubertal children

Journal of Pediatric Endocrinology and Metabolism ◽

10.1515/jpem-2017-0182 ◽

2018 ◽

Vol 31 (1) ◽

pp. 45-51 ◽

Cited By ~ 4

Author(s):

Paola Di Filippo ◽

Alessandra Scaparrotta ◽

Daniele Rapino ◽

Tommaso de Giorgis ◽

Marianna Immacolata Petrosino ◽

...

Keyword(s):

Insulin Resistance ◽

Lung Function ◽

Statistical Significance ◽

Serum Levels ◽

Forced Expiratory Volume ◽

Normal Weight ◽

Model Assessment ◽

Obese Children ◽

Asthmatic Children ◽

Insulin Resistant

AbstractBackground:Recent findings have supposed that the underlying association between the increased prevalence of both asthma and obesity may be insulin resistance (IR).Methods:Insulin and glucose serum levels were analyzed to calculate the homeostatic model assessment of insulin resistance (HOMA-IR) for IR in 98 pre-pubertal children. Lung function and allergy status evaluation were performed. The study population was divided into four groups: (1) obese asthmatic children (ObA); (2) normal-weight asthmatic children (NwA); (3) normal-weight non-asthmatic children (Nw) and (4) obese non-asthmatic children (Ob).Results:Forced expiratory volume in 1 s (FEV1) was slightly lower in obese subjects compared with normal-weight subjects and forced vital capacity (FVC) appeared lower in asthmatics, whereas between non-asthmatics subjects, it was lower in the obese group than in the normal-weight one. The post hoc analysis revealed a statistically significant reduction in FEV1, peak expiratory flow (PEF), forced expiratory flows (FEF) between 50% and 25% of the FVC (FEF50and FEF25) between ObA and Nw and in FEV1, FVC, PEF, FEF50and FEF25between NwA and Nw, but no statistically significant differences of lung function parameters were observed between ObA and NwA. We found an inverse relationship between HOMA-IR and all spirometric parameters, although without any statistical significance. We also observed a significantly lower FVC in insulin-resistant children (HOMA-IR>95th percentile) (p=0.03).Conclusions:This study suggests that lung function could be early altered in obese children, already in pre-pubertal age. Although IR should not manifest its effects on lungs in pre-pubertal obese children, the prevention or treatment of obesity in the pre-pubertal period may prevent definitive negative effects on lungs.

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RBP4: A Culprit for Insulin Resistance in End Stage Renal Disease That Can Be Cleared by Hemodiafiltration

BioMed Research International ◽

10.1155/2017/7270595 ◽

2017 ◽

Vol 2017 ◽

pp. 1-8 ◽

Cited By ~ 1

Author(s):

Fabrizio Grosjean ◽

Pasquale Esposito ◽

Rosario Maccarrone ◽

Carmelo Libetta ◽

Antonio Dal Canton ◽

...

Keyword(s):

Insulin Resistance ◽

Adipose Tissue ◽

Kidney Transplant ◽

Glucose Transporter ◽

Serum Levels ◽

Tissue Expression ◽

Serum Glucose ◽

Retinol Binding Protein ◽

Retinol Binding Protein 4 ◽

Glut4 Expression

Introduction. Retinol Binding Protein 4 (RBP4) is mainly excreted by the kidney and plays a pivotal role in insulin resistance (IR). In our study, we evaluated the association between RBP4 and IR in hemodialysis subjects (HD). We also assessed how circulating RBP4 could be influenced by kidney transplant or different dialytic techniques.Methods. RBP4 serum levels were evaluated in HD (n=16) and matched healthy controls (C;n=16). RBP4 and glucose transporter type 4 (GLUT4) mRNA expressions were also determined in adipose tissue. Circulating RBP4 was evaluated after kidney transplant (n=7) and in hemodialysis patients (n=10) enrolled in a cross-over study treated with standard bicarbonate dialysis (BD) or hemodiafiltration (HDF).Results. HOMA index (P<0.05) and serum RBP4 (P<0.005) were higher in HD compared to C. RBP4 levels positively correlated with fasting serum glucose (P<0.05). RBP4 mRNA was lower in HD compared to C (P<0.05) and positively correlated with kidney function (P<0.05) and GLUT4 mRNA (P<0.001). Transplant or HDF reduced circulating RBP4 (P<0.01andP<0.05, resp.). Our results demonstrate that IR is associated with high circulating RBP4 and that suppressed RBP4 adipose tissue expression is accompanied by reduced GLUT4 expression in HD. Renal transplantation or HDF are effective in lowering serum RBP4 levels.

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The Effects of Gymnema sylvestre in High-Fat Diet-Induced Metabolic Disorders

The American Journal of Chinese Medicine ◽

10.1142/s0192415x17500434 ◽

2017 ◽

Vol 45 (04) ◽

pp. 813-832 ◽

Cited By ~ 5

Author(s):

Hyeon-Jeong Kim ◽

Sanghwa Kim ◽

Ah Young Lee ◽

Yoonjeong Jang ◽

Orkhonselenge Davaadamdin ◽

...

Keyword(s):

Insulin Resistance ◽

Body Weight ◽

Adipose Tissue ◽

Dietary Supplement ◽

High Fat Diet ◽

Liver Steatosis ◽

Integrated Approach ◽

Serum Levels ◽

Gymnema Sylvestre ◽

High Fat

This study used an integrated approach to investigate the effects of Gymnema sylvestre (GS) extract as a functional dietary supplement with a high-fat diet. This approach examined insulin resistance, the dysfunction of adipose tissue, and liver steatosis. Male C57BL/6J mice were fed a normal chow or high-fat diet (HFD) for the acute and chronic study, in addition to GS in different doses (100, 250 and 500[Formula: see text]mg/kg body weight). Their body composition changes, serum lipid and glucose parameters, adipose and liver tissue histology, and gene expression were measured. It was found that GS significantly suppressed the increase of body weight, serum levels of lipid, insulin and leptin, and adipose tissue, and liver inflammation. GS also demonstrated hypoglycemic effects due to the amylase inhibition activity. Our results support the existence of a relationship between the HFD induced insulin resistance, adipose dysfunction and liver steatosis. In conclusion, GS works as a functional dietary supplement with preventative effects against metabolic disorder.

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Abstract 1123: Critical Role Of Adipose Senescence In Insulin Resistance And Vascular Dysfunction

Circulation ◽

10.1161/circ.116.suppl_16.ii_226-a ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Masayuki Orimo ◽

Tohru Minamino ◽

Hideyuki Miyauchi ◽

Kaoru Tateno ◽

Sho Okada ◽

...

Keyword(s):

Insulin Resistance ◽

Adipose Tissue ◽

Inflammatory Cytokines ◽

Cellular Senescence ◽

Vascular Dysfunction ◽

Critical Role ◽

Serum Levels ◽

P53 Expression ◽

Deficient Mice ◽

Pro Inflammatory Cytokines

Cellular senescence is originally described as the finite replicative lifespan of human somatic cells in culture. As a consequence of semi-conservative DNA replication, the extreme terminals of the chromosomes are not duplicated completely, resulting in successive shortening of telomeres with each cell division. Telomerase is a ribonucleoprotein that adds telomeres to the ends of chromosomes. Critically short telomeres are thought to trigger DNA damage response, thereby inducing cellular senescence. Accumulating evidence has suggested that senescent cells promote aging phenotypes or age-related pathologies. Here we show that adipose senescence is critically involved in the regulation of insulin resistance that underlies age-associated cardiovascular disease. The later generation of telomerase-deficient mice with short telomeres exhibited insulin resistance and vascular dysfunction when fed on a high-calorie diet. Adipose tissue of these mice revealed senescence-like phenotypes such as an increase in neutral β galactosidase activity and upregulation of p53 and pro-inflammatory cytokines. Serum levels of pro-inflammatory cytokines were markedly elevated in telomerase-deficient mice and treatment of these mice with a neutralizing antibody against TNF-α significantly improved insulin and glucose intolerance. Removal of senescent adipose tissue reduced serum levels of pro-inflammatory cytokines and thereby improved insulin resistance in telomerase-deficient mice. Conversely, implantation of senescent adipose tissue to wild-type mice impaired insulin sensitivity and glucose tolerance in recipients. Introduction of telomere dysfunction to young adipose tissue markedly upregulated p53 expression and increased the production of pro-inflammatory cytokines. Inhibition of p53 activity significantly improved senescence-like phenotypes of adipose tissue, insulin resistance, and vascular dysfunction in telomerase-deficient mice. These results disclose a novel mechanism of insulin resistance and suggest that adipose senescence is a potential therapeutic target for the treatment of diabetes and diabetic vasculopathy.

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S100B Serum Levels in Schizophrenia Are Presumably Related to Visceral Obesity and Insulin Resistance

Cardiovascular Psychiatry and Neurology ◽

10.1155/2010/480707 ◽

2010 ◽

Vol 2010 ◽

pp. 1-11 ◽

Cited By ~ 18

Author(s):

Johann Steiner ◽

Aye Mu Myint ◽

Kolja Schiltz ◽

Sabine Westphal ◽

Hans-Gert Bernstein ◽

...

Keyword(s):

Insulin Resistance ◽

Adipose Tissue ◽

Glucose Metabolism ◽

Nervous Tissue ◽

Surrogate Marker ◽

Visceral Obesity ◽

Serum Levels ◽

Blood Levels ◽

Elevated Blood ◽

Metabolic Disturbances

Elevated blood levels of S100B in schizophrenia have so far been mainly attributed to glial pathology, as S100B is produced by astro- and oligodendroglial cells and is thought to act as a neurotrophic factor with effects on synaptogenesis, dopaminergic and glutamatergic neutrotransmission. However, adipocytes are another important source of S100B since the concentration of S100B in adipose tissue is as high as in nervous tissue. Insulin is downregulating S100B in adipocytes, astrocyte cultures and rat brain. As reviewed in this paper, our recent studies suggest that overweight, visceral obesity, and peripheral/cerebral insulin resistance may be pivotal for at least part of the elevated S100B serum levels in schizophrenia. In the context of this recently identified framework of metabolic disturbances accompanying S100B elevation in schizophrenia, it rather has to be attributed to systemic alterations in glucose metabolism than to be considered a surrogate marker for astrocyte-specific pathologies.

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Altered serum level of metabolic and endothelial factors in patients with systemic sclerosis

Archives of Dermatological Research ◽

10.1007/s00403-019-01993-y ◽

2019 ◽

Vol 312 (6) ◽

pp. 453-458

Author(s):

Anna Stochmal ◽

Joanna Czuwara ◽

Michał Zaremba ◽

Lidia Rudnicka

Keyword(s):

Adipose Tissue ◽

Systemic Sclerosis ◽

Serum Level ◽

Elevated Serum ◽

Serum Levels ◽

Enzyme Linked Immunosorbent Assay ◽

Vascular Abnormalities ◽

Endothelin 1 ◽

Fibrotic Process ◽

Galectin 3

Abstract Systemic sclerosis (SSc) is a chronic connective tissue disease characterized by progressive fibrosis, vascular impairment and immune abnormalities. In recent years, adipokines (mediators synthetized by adipose tissue) have been indicated as a possible missing link in the pathogenesis of SSc. The aim of this study was to investigate the serum concentration of metabolic adipose tissue factors: adiponectin, resistin, leptin and endothelial proteins: endothelin-1, fractalkine and galectin-3 in patients with systemic sclerosis. The study included 100 patients with confirmed SSc diagnosis and 20 healthy individuals. The concentration of respective proteins was determined by enzyme-linked immunosorbent assay. The following markers showed statistically significant increased mean concentrations in patients with SSc in comparison to healthy control: resistin (13.41 vs 8.54 ng/mL; P = 0.0012), endothelin-1 (1.99 vs 1.31 pg/mL; P = 0.0072) and fractalkine (2.93 vs 1.68 ng/mL; P = 0.0007). Elevated serum levels of galectin-3 (4.54 vs 3.26 ng/mL; P = 0.0672) and leptin (19,542 vs 14,210 pg/mL; P = 0.1817) were observed. Decreased concentration of adiponectin was found in patients with SSc (5150 vs 8847 pg/mL; P = 0.0001). Fractalkine and galectin-3 levels were significantly higher in diffuse cutaneous SSc than limited cutaneous SSc subset (3.93 ng/mL vs 2.58 ng/mL, P = 0.0018; 6.86 ng/mL vs 3.78 ng/mL, P = 0.0008, respectively) and correlated positively with modified Rodnan Skin Score in total SSc patients (r = 0.376, P = 0.0009; r = 0.236, P = 0.018, respectively). In conclusion, an increased serum level of resistin associated with increased endothelin-1 and fractalkine level and decreased adiponectin level may indicate a significant role of the adipose tissue in the development and progression of vascular abnormalities in patients with systemic sclerosis. Fractalkine and galectin-3 may participate in promoting and exacerbating the fibrotic process in SSc.

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Glycemic index differences of high-fat diets modulate primarily lipid metabolism in murine adipose tissue

Physiological Genomics ◽

10.1152/physiolgenomics.00042.2011 ◽

2011 ◽

Vol 43 (15) ◽

pp. 942-949 ◽

Cited By ~ 10

Author(s):

Evert M. van Schothorst ◽

Annelies Bunschoten ◽

Eline Verlinde ◽

Patrick Schrauwen ◽

Jaap Keijer

Keyword(s):

Insulin Resistance ◽

Adipose Tissue ◽

Insulin Sensitivity ◽

Glycemic Index ◽

Molecular Mechanisms ◽

Serum Levels ◽

Whole Body ◽

High Fat ◽

Beneficial Effects ◽

Ppar Γ

A low vs. high glycemic index of a high-fat (HF) diet (LGI and HGI, respectively) significantly retarded adverse health effects in adult male C57BL/6J mice, as shown recently (Van Schothorst EM, Bunschoten A, Schrauwen P, Mensink RP, Keijer J. FASEB J 23: 1092–1101, 2009). The LGI diet enhanced whole body insulin sensitivity and repressed HF diet-induced body and white adipose tissue (WAT) weight gain, resulting in significantly reduced serum leptin and resistin levels and increased adiponectin levels. We questioned how WAT is modulated and characterized the molecular mechanisms underlying the glycemic index-mediated effects using whole genome microarrays. This showed that the LGI diet mainly exerts its beneficial effects via substrate metabolism, especially fatty acid metabolism. In addition, cell adhesion and cytoskeleton remodeling showed reduced expression, in line with lower WAT mass. An important transcription factor showing enhanced expression is PPAR-γ. Furthermore, serum levels of triglycerides, total cholesterol, and HDL- and LDL-cholesterol were all significantly reduced by LGI diet, and simultaneously muscle insulin sensitivity was significantly increased as analyzed by protein kinase B/Akt phosphorylation. Cumulatively, even though these mice were fed an HF diet, the LGI diet induced significantly favorable changes in metabolism in WAT. These effects suggest a partial overlap with pharmacological approaches by thiazolidinediones to treat insulin resistance and statins for hypercholesterolemia. It is therefore tempting to speculate that such a dietary approach might beneficially support pharmacological treatment of insulin resistance or hypercholesterolemia in humans.

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Apocynin Improves Insulin Resistance through Suppressing Inflammation in High-Fat Diet-Induced Obese Mice

Mediators of Inflammation ◽

10.1155/2010/858735 ◽

2010 ◽

Vol 2010 ◽

pp. 1-9 ◽

Cited By ~ 11

Author(s):

Ran Meng ◽

Da-Long Zhu ◽

Yan Bi ◽

Dong-Hui Yang ◽

Ya-Ping Wang

Keyword(s):

Insulin Resistance ◽

Adipose Tissue ◽

Mrna Expression ◽

High Fat Diet ◽

Serum Levels ◽

Tolerance Test ◽

Inflammatory Factors ◽

High Fat ◽

Monocyte Chemoattractant Protein 1 ◽

Necrosis Factor

We investigated the effects of apocynin on high-fat diet- (HFD-) induced insulin resistance in C57BL/6 mice. After 12 weeks of HFD, the mice that exhibited insulin resistance then received 5 weeks of apocynin (2.4 g/L, in water). Following apocynin treatment, fasting glucose, insulin, and glucose tolerance test showed significant improvement in insulin sensitivity in HFD-fed mice. We demonstrated that serum levels of tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6), and leptin were remarkably reduced with apocynin treatment. We also found that mRNA expression of TNF-α, IL-6, and monocyte chemoattractant protein-1 (MCP-1) in the liver and mRNA expression of TNF-α, IL-6, MCP-1, and leptin in adipose tissue were suppressed by apocynin. Furthermore, the activity of transcription factor NF-κB in the liver was significantly suppressed with apocynin treatment. These results suggest that apocynin may reduce inflammatory factors in the blood, liver, and adipose tissue, resulting in amelioration of insulin resistance in HFD-fed mice.

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