Resistin has been originally identified as an adipokine that links obesity to insulin resistance in mice. In our previous studies in spontaneously hypertensive rats (SHR) expressing a nonsecreted form of mouse resistin (Retn) transgene specifically in adipose tissue (SHR-Retn), we have observed an increased lipolysis and serum free fatty acids, ectopic fat accumulation in muscles, and insulin resistance. Recently, brown adipose tissue (BAT) has been suggested to play an important role in the pathogenesis of metabolic disturbances. In the current study, we have analyzed autocrine effects of transgenic resistin on BAT glucose and lipid metabolism and mitochondrial function in the SHR-Retn vs. nontransgenic SHR controls. We observed that interscapular BAT isolated from SHR-Retn transgenic rats compared with SHR controls showed a lower relative weight (0.71 ± 0.05 vs. 0.91 ± 0.08 g/100 g body wt, P < 0.05), significantly reduced both basal and insulin stimulated incorporation of palmitate into BAT lipids (658 ± 50 vs. 856 ± 45 and 864 ± 47 vs. 1,086 ± 35 nmol/g/2 h, P ≤ 0.01, respectively), and significantly decreased palmitate oxidation (37.6 ± 4.5 vs. 57 ± 4.1 nmol/g/2 h, P = 0.007) and glucose oxidation (277 ± 34 vs. 458 ± 38 nmol/g/2 h, P = 0.001). In addition, in vivo microPET imaging revealed significantly reduced (18)F-FDG uptake in BAT induced by exposure to cold in SHR-Retn vs. control SHR (232 ± 19 vs. 334 ± 22 kBq/ml, P < 0.05). Gene expression profiles in BAT identified differentially expressed genes involved in skeletal muscle and connective tissue development, inflammation and MAPK and insulin signaling. These results provide evidence that autocrine effects of resistin attenuate differentiation and activity of BAT and thus may play a role in the pathogenesis of insulin resistance in the rat.

• Klíčová slova
• autocrine, brown adipose tissue, resistin, spontaneously hypertensive rat, transgenic,
• MeSH
• autokrinní signalizace genetika   fyziologie   MeSH
• glukosa metabolismus   MeSH
• hnědá tuková tkáň metabolismus   fyziologie   MeSH
• inzulin metabolismus   MeSH
• inzulinová rezistence fyziologie   MeSH
• kosterní svaly metabolismus   fyziologie   MeSH
• krysa rodu Rattus MeSH
• kyseliny mastné neesterifikované metabolismus   MeSH
• metabolismus lipidů fyziologie   MeSH
• mitochondrie genetika   fyziologie   MeSH
• myši inbrední BALB C MeSH
• myši MeSH
• obezita metabolismus   patofyziologie   MeSH
• oxidace-redukce MeSH
• palmitany metabolismus   MeSH
• potkani inbrední SHR MeSH
• potkani transgenní MeSH
• resistin genetika   MeSH
• transkriptom genetika   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• glukosa MeSH
• inzulin MeSH
• kyseliny mastné neesterifikované MeSH
• palmitany MeSH
• resistin MeSH

Cancer of endometrium (CAE) is the most common gynecologic malignancy in industrialized nations. Increased resistin levels, an adipocytokine produced by adipose tissue and macrophages, have been considered as a risk factor in gastric, colon and breast cancer, recently. No studies associating resistin levels with endometrial cancer have been done so far. The purpose of this case-control study was to determine the relationship between serum circulating resistin levels and resistin gene -420C>G (rs3219175) variant in endometrial cancer patients. 37 Caucasian female patients and 39 healthy controls were enrolled in this study. Difference in resistin levels between age and BMI matched patients group (mean 24.2 ng/ml) and control subjects (mean 10.1 ng/ml) were statistically significant (p <001). We also determined single nucleotide polymorphism -420C>G (rs3219175) within resistin gene and no significant association between resistin levels and investigated polymorphism was found. Furthermore, no significant association between higher resistin levels and diabetes mellitus 2, body mass index, smoking or age have been observed within studied groups. To our knowledge, this is the first study examining the relationship between serum resistin levels and endometrial cancer and our results show, that patients with endometrial cancer have significantly increased circulating levels of resistin compared to control subjects.

• MeSH
• dospělí MeSH
• genotyp MeSH
• index tělesné hmotnosti MeSH
• kojenec MeSH
• lidé středního věku MeSH
• lidé MeSH
• nádory endometria krev   etiologie   MeSH
• resistin krev   genetika   MeSH
• senioři MeSH
• Check Tag
• dospělí MeSH
• kojenec MeSH
• lidé středního věku MeSH
• lidé MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• resistin MeSH
• RETN protein, human MeSH Prohlížeč

Increased circulating levels of resistin have been proposed as a possible link between obesity and insulin resistance; however, many of the potential metabolic effects of resistin remain to be investigated, including systemic versus local resistin action. We investigated potential autocrine effects of resistin on lipid and glucose metabolism in 2- and 16-mo-old transgenic spontaneously hypertensive rats (SHR) expressing a nonsecreted form of mouse resistin under control of the aP2 promoter. To search for possible molecular mechanisms, we compared gene expression profiles in adipose tissue in 6-wk-old transgenic SHR versus control rats, before development of insulin resistance, by digital transcriptional profiling using high-throughput sequencing. Both young and old transgenic rats showed moderate expression of the resistin transgene in adipose tissue but had serum resistin levels similar to control SHR and undetectable levels of transgenic resistin in the circulation. Young transgenic rats exhibited mild glucose intolerance. In contrast, older transgenic rats displayed marked glucose intolerance in association with near total resistance of adipose tissue to insulin-stimulated glucose incorporation into lipids (6 ± 2 vs. 77 ± 19 nmol glucose·g(-1)·2 h(-1), P < 0.00001). Ingenuity Pathway Analysis of differentially expressed genes revealed calcium signaling, Nuclear factor-erythroid 2-related factor-2 (NRF2)-mediated oxidative stress response, and actin cytoskeletal signaling canonical pathways as those most significantly affected. Analysis using DAVID software revealed oxidative phosphorylation, glutathione metabolism, pyruvate metabolism, and peroxisome proliferator-activated receptor (PPAR) signaling as top Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. These results suggest that with increasing age autocrine effects of resistin in fat tissue may predispose to diabetes in part by impairing insulin action in adipose tissue.

• MeSH
• glukózový toleranční test MeSH
• inzulinová rezistence genetika   fyziologie   MeSH
• krysa rodu Rattus MeSH
• polymerázová řetězová reakce MeSH
• potkani inbrední SHR MeSH
• potkani transgenní MeSH
• resistin genetika   metabolismus   MeSH
• stanovení celkové genové exprese metody   MeSH
• stárnutí genetika   metabolismus   MeSH
• tuková tkáň metabolismus   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Research Support, N.I.H., Extramural MeSH
• Názvy látek
• resistin MeSH

• MeSH
• adiponektin genetika   MeSH
• energetický metabolismus genetika   MeSH
• fenotyp MeSH
• genetická predispozice k nemoci MeSH
• jednonukleotidový polymorfismus * MeSH
• lidé MeSH
• mentální anorexie genetika   metabolismus   MeSH
• obezita MeSH
• resistin genetika   MeSH
• výzkumný projekt MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• dopisy MeSH
• komentáře MeSH
• Názvy látek
• adiponektin MeSH
• ADIPOQ protein, human MeSH Prohlížeč
• resistin MeSH
• RETN protein, human MeSH Prohlížeč

OBJECTIVE: The number of patients with end-stage renal disease (ESRD) is rising and these patients are at higher risk of cardiovascular disease. We studied the role of hormonal production of adipose tissue in the development of chronic inflammation in patients with ESRD before kidney transplantation. METHODS: Fifteen women with ESRD and 17 healthy women (control) underwent single blood drawing and visceral and subcutaneous adipose tissue sampling during surgery (kidney transplantation in the ESRD group or cholecystectomy in the control group). Serum concentrations of C-reactive protein, interleukin-6, tumor necrosis factor-alpha, leptin, adiponectin, resistin, monocyte chemoattractant protein-1 were measured. Messenger RNA expression of the same hormones, adiponectin receptors 1 and 2 and immunocompetent cell marker CD68 in subcutaneous and visceral samples were measured using real-time polymerase chain reaction. Adipose tissue was examined immunohistochemically for CD68-positive cells. RESULTS: Serum concentrations of C-reactive protein, adiponectin, resistin, interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 were significantly higher in the ESRD versus control group. Subcutaneous and visceral mRNA expressions of tumor necrosis factor-alpha and CD68 were significantly increased in the ESRD versus control group. Adiponectin receptor-1 and monocyte chemoattractant protein-1 mRNA expressions were significantly higher in visceral but not in subcutaneous adipose tissue of the ESRD group. Messenger RNA expressions of resistin, leptin, adiponectin, interleukin-6, and adiponectin receptor-2 in both fat depots did not significantly differ between groups. Increased infiltration of subcutaneous and visceral adipose tissue with CD68-positive immunocompetent cells was found in the ESRD group by histologic examination. CONCLUSION: Subcutaneous and visceral adipose tissues in ESRD express higher amounts of proinflammatory cytokines and may play a role in the development of systemic inflammation.

• MeSH
• adiponektin genetika   metabolismus   MeSH
• antigeny diferenciační myelomonocytární metabolismus   MeSH
• C-reaktivní protein metabolismus   MeSH
• CD antigeny metabolismus   MeSH
• chemokin CCL2 genetika   metabolismus   MeSH
• chronické selhání ledvin metabolismus   MeSH
• cytokiny metabolismus   MeSH
• interleukin-6 genetika   metabolismus   MeSH
• lidé středního věku MeSH
• lidé MeSH
• mediátory zánětu metabolismus   MeSH
• messenger RNA biosyntéza   MeSH
• nitrobřišní tuk metabolismus   MeSH
• podkožní tuk metabolismus   MeSH
• receptory adiponektinu biosyntéza   genetika   MeSH
• resistin genetika   metabolismus   MeSH
• TNF-alfa krev   MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adiponektin MeSH
• ADIPOR1 protein, human MeSH Prohlížeč
• antigeny diferenciační myelomonocytární MeSH
• C-reaktivní protein MeSH
• CD antigeny MeSH
• CD68 antigen, human MeSH Prohlížeč
• chemokin CCL2 MeSH
• cytokiny MeSH
• interleukin-6 MeSH
• mediátory zánětu MeSH
• messenger RNA MeSH
• receptory adiponektinu MeSH
• resistin MeSH
• TNF-alfa MeSH

Genes for adiponectin and resistin are candidate genes of insulin resistance and type 2 diabetes mellitus. The aim of our study was to determine the frequency of single nucleotide polymorphisms (SNP) 45T>G and 276G>T of the adiponectin gene and 62G>A and -180C>G of the resistin gene in patients with obesity (OB), anorexia nervosa (AN) and in control healthy normal-weight women (NW) and to study the influence of particular genotypes on serum concentrations of these hormones and on insulin sensitivity. Serum adiponectin, resistin, tumor necrosis factor alpha (TNF-alpha), insulin, cholesterol, glycated hemoglobin (HbA1c) and blood glucose levels were measured in 77 patients with OB, 28 with AN and 38 NW. DNA analysis was carried out by polymerase chain reaction with restriction analysis of PCR product. The presence of SNP ADP+276 G>T allele was accompanied by higher cholesterol levels in AN patients, higher adiponectin concentrations in OB patients and lower HbA1c levels in NW. SNP of the resistin gene 62G>A was associated with lower HbA1c in NW and higher cholesterol concentrations in OB group. The carriers of the minor G allele in the position -180 of the resistin gene within AN group had significantly higher BMI relative to non-carriers. We conclude that polymorphisms in adiponectin and resistin genes can contribute to metabolic phenotype of patients with obesity and anorexia nervosa.

• MeSH
• adiponektin genetika   MeSH
• cholesterol krev   MeSH
• DNA biosyntéza   genetika   MeSH
• dospělí MeSH
• ELISA MeSH
• fenotyp MeSH
• glykovaný hemoglobin metabolismus   MeSH
• index tělesné hmotnosti MeSH
• jednonukleotidový polymorfismus MeSH
• lidé MeSH
• mentální anorexie genetika   metabolismus   MeSH
• obezita genetika   metabolismus   MeSH
• polymerázová řetězová reakce s reverzní transkripcí MeSH
• polymorfismus délky restrikčních fragmentů MeSH
• polymorfismus genetický fyziologie   MeSH
• resistin genetika   MeSH
• TNF-alfa krev   MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adiponektin MeSH
• cholesterol MeSH
• DNA MeSH
• glykovaný hemoglobin MeSH
• resistin MeSH
• TNF-alfa MeSH

OBJECTIVE: To study the influence of chronic malnutrition in patients with anorexia nervosa on endocrine function of adipose tissue on both circulating and subcutaneous fat mRNA expression level. PATIENTS AND DESIGN: A total of 12 patients with anorexia nervosa and 18 normal weight age-matched women underwent anthropometric examination, single blood drawing and subcutaneous adipose tissue biopsy. MEASUREMENTS: Serum concentrations of high-sensitive CRP (hsCRP), leptin, soluble leptin receptor, adiponectin, resistin, interleukin-6 and insulin were measured by Luminex, enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA) kits. Subcutaneous adipose tissue mRNA expression of the same adipokines, adiponectin receptors 1 and 2 and immunocompetent cells marker CD68 was measured by real-time polymerase chain reaction (PCR). RESULTS: Decreased body fat content of patients with anorexia nervosa was accompanied by reduced hsCRP, leptin and increased adiponectin and soluble leptin receptor. Resistin, interleukin-6 and insulin levels did not differ from those of the control group. Fat mRNA adiponectin, leptin, interleukin-6 and CD68 expression was reduced, resistin mRNA expression was increased and adiponectin receptor 1 and 2 expression were unchanged as compared to the control group. CONCLUSIONS: Local perturbations in resistin, adiponectin and interleukin-6 mRNA expression in subcutaneous adipose tissue are not reflected by its circulating levels. These changes could be involved in some local metabolic disturbances in subcutaneous adipose tissue of anorexia nervosa patients.

• MeSH
• adiponektin krev   genetika   MeSH
• antigeny diferenciační myelomonocytární genetika   MeSH
• C-reaktivní protein analýza   MeSH
• CD antigeny genetika   MeSH
• dospělí MeSH
• exprese genu MeSH
• fyziologická adaptace MeSH
• interleukin-6 genetika   MeSH
• inzulin krev   MeSH
• krevní glukóza analýza   MeSH
• leptinové receptory krev   MeSH
• lidé MeSH
• mentální anorexie imunologie   metabolismus   MeSH
• messenger RNA analýza   MeSH
• neparametrická statistika MeSH
• parakrinní signalizace * MeSH
• podkožní tuk chemie   imunologie   metabolismus   MeSH
• podvýživa imunologie   metabolismus   MeSH
• resistin krev   genetika   MeSH
• studie případů a kontrol MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• srovnávací studie MeSH
• Názvy látek
• adiponektin MeSH
• antigeny diferenciační myelomonocytární MeSH
• C-reaktivní protein MeSH
• CD antigeny MeSH
• CD68 antigen, human MeSH Prohlížeč
• interleukin-6 MeSH
• inzulin MeSH
• krevní glukóza MeSH
• leptinové receptory MeSH
• messenger RNA MeSH
• resistin MeSH

OBJECTIVE: The potential insulin-sensitizing function of angiotensin II type 1 receptor blockade (ARB) with regard to selected adipokines is not fully explained so far. Our study aimed to explore the influence of acute hyperinsulinaemia and acutely induced ARB on resistin and adiponectin concentrations and expressions in healthy subjects. DESIGN AND METHODS: Plasma adipokines were measured: 1) at 0, 30 and 240 min of hyperinsulinaemic (1 mU/kg per min) euglycaemic (5 mmol/l) clamp (HEC), and 2) during HEC after acute ARB (losartan 200 mg; AT-HEC) using the same protocol, in eight healthy subjects. Needle biopsy of abdominal s.c. fat was performed at 0, 30 and 240 min of both clamps to assess the adipokines' expressions. RESULTS: Comparing the glucose disposals of HEC and AT-HEC, no difference in insulin sensitivity was found. Plasma resistin increased equally during HEC and AT-HEC (P < 0.05). The expression of resistin in s.c. fat increased during HEC (P < 0.05), while no significant changes in expression were observed during AT-HEC. Plasma levels of adiponectin did not change during both clamps. Adiponectin expression increased during HEC (P < 0.05), while it did not change during AT-HEC. CONCLUSIONS: In healthy subjects, acute hyperinsulinaemia is associated with an increase in plasma resistin independently of ARB, while plasma adiponectin is not influenced by insulin or ARB. The expressions of both resistin and adiponectin in s.c. adipose tissue are stimulated by acute hyperinsulinaemia, whereas losartan attenuates their insulin-stimulated expressions. This suggests a potential effect of losartanon adipokines' expression.

• MeSH
• adiponektin krev   genetika   metabolismus   MeSH
• blokátory receptorů AT1 pro angiotensin II aplikace a dávkování   MeSH
• dospělí MeSH
• exprese genu účinky léků   MeSH
• fixní kombinace léků MeSH
• glykemický clamp MeSH
• hyperinzulinismus chemicky indukované   MeSH
• inzulin aplikace a dávkování   MeSH
• lidé MeSH
• losartan aplikace a dávkování   MeSH
• nitrobřišní tuk účinky léků   metabolismus   MeSH
• receptor angiotensinu typ 1 fyziologie   MeSH
• resistin krev   genetika   metabolismus   MeSH
• zdraví MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• randomizované kontrolované studie MeSH
• Názvy látek
• adiponektin MeSH
• ADIPOQ protein, human MeSH Prohlížeč
• blokátory receptorů AT1 pro angiotensin II MeSH
• fixní kombinace léků MeSH
• inzulin MeSH
• losartan MeSH
• receptor angiotensinu typ 1 MeSH
• resistin MeSH
• RETN protein, human MeSH Prohlížeč

BACKGROUND: Adiponectin and resistin are hormones that may represent a link between obesity and insulin resistance. Genes for these hormones are new candidate genes of insulin resistance and type 2 diabetes mellitus. The aim of our study was to determine the frequency of single nucleotide polymorphisms 45T > G and 276T > G of adiponectin gene and 62G > A and -180C > G of resistin gene in patients with obesity, anorexia nervosa and in lean women and to study the influence of particular genotypes on serum concentrations of these hormones. METHODS AND RESULTS: Serum adiponectin, resistin, TNF-alfa and insulin levels were measured in 51 patients with obesity, 17 with anorexia nervosa and 17 lean women. DNA analysis was carried out by means of polymerase chain reaction (PCR) with restriction analysis of PCR product (RFLP). Adiponectin levels were lowest in obese women and highest in anorexia nervosa patients. Resistin concentrations were lowest in anorexia nervosa and highest in obese patients. Genotype analysis within respective groups showed no differences in assessed parameters when comparing different adiponectin and resistin polymorphisms. The only difference detected was significantly higher BMI in G/G genotype relative to T allele carries in 276 position of ADP gene in control group (23.48 +/- 0.85 vs. 19,7 +/- 0.95, p < 0.05). In anorexia nervosa patients, frequency of G allele in RETN -180 polymorphism was significantly higher relative to control group (p < 0.05). CONCLUSIONS: Polymorphisms 45T > G a 276T > G of ADP gene and 62G>A and -180C > G RETN gene did not influence serum ADP and RETN concentrations. BMI was influenced by T allele presence in 276 position of ADP gene in control group only. Anorexia nervosa patients had higher frequency of G allele of RETN -180 polymorphism compared to healthy women.

• MeSH
• adiponektin krev   genetika   MeSH
• jednonukleotidový polymorfismus * MeSH
• lidé MeSH
• mentální anorexie krev   genetika   MeSH
• obezita krev   genetika   MeSH
• resistin krev   genetika   MeSH
• Check Tag
• lidé MeSH
• ženské pohlaví MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adiponektin MeSH
• resistin MeSH

We studied the effect of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activation on serum concentrations and tissue expression of resistin, adiponectin, and adiponectin receptor-1 and -2 (AdipoR1 and AdipoR2) mRNA in normal mice and mice with insulin resistance induced by lipogenic, simple-carbohydrate diet (LD). Sixteen weeks of LD feeding induced obesity with liver steatosis and increased insulin levels but did not significantly affect circulating adiponectin or resistin. Treatment with PPAR-alpha agonist fenofibrate decreased body weight and fat pad weight and ameliorated liver steatosis in LD-fed mice with concomitant reduction in blood glucose, free fatty acid, triglyceride, serum insulin levels, and homeostasis model assessment index values. Euglycemic-hyperinsulinemic clamp demonstrated the development of whole-body and liver insulin resistance in LD-fed mice, which were both normalized by fenofibrate. Fenofibrate treatment markedly increased circulating resistin levels on both diets and adiponectin levels in chow-fed mice only. Fat adiponectin mRNA expression was not affected by fenofibrate treatment. Resistin mRNA expression increased in subcutaneous but not gonadal fat after fenofibrate treatment. In addition to fat, a significant amount of adiponectin mRNA was also expressed in the muscle. This expression markedly increased after fenofibrate treatment in chow- but not in LD-fed mice. Adipose tissue expression of AdipoR1 mRNA was significantly reduced in LD-fed mice and increased after fenofibrate treatment. In conclusion, PPAR-alpha activation ameliorated the development of insulin resistance in LD-fed mice despite a major increase in serum resistin levels. This effect could be partially explained by increased AdipoR1 expression in adipose tissue after fenofibrate treatment.

• MeSH
• adiponektin krev   genetika   MeSH
• dieta MeSH
• dietní sacharidy aplikace a dávkování   MeSH
• exprese genu účinky léků   MeSH
• fenofibrát aplikace a dávkování   MeSH
• glykemický clamp MeSH
• hmotnostní úbytek účinky léků   MeSH
• inzulin krev   farmakologie   MeSH
• inzulinová rezistence * MeSH
• játra chemie   účinky léků   MeSH
• kosterní svaly chemie   MeSH
• krevní glukóza analýza   MeSH
• kyseliny mastné neesterifikované analýza   MeSH
• lipidy biosyntéza   MeSH
• messenger RNA analýza   MeSH
• myši inbrední C57BL MeSH
• myši MeSH
• obezita krev   etiologie   patofyziologie   MeSH
• PPAR alfa agonisté   fyziologie   MeSH
• receptory adiponektinu MeSH
• receptory buněčného povrchu genetika   MeSH
• resistin krev   genetika   MeSH
• triglyceridy krev   MeSH
• tuková tkáň chemie   patologie   MeSH
• velikost orgánu účinky léků   MeSH
• ztučnělá játra krev   farmakoterapie   etiologie   MeSH
• zvířata MeSH
• Check Tag
• mužské pohlaví MeSH
• myši MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• adiponectin receptor 1, mouse MeSH Prohlížeč
• adiponectin receptor 2, mouse MeSH Prohlížeč
• adiponektin MeSH
• dietní sacharidy MeSH
• fenofibrát MeSH
• inzulin MeSH
• krevní glukóza MeSH
• kyseliny mastné neesterifikované MeSH
• lipidy MeSH
• messenger RNA MeSH
• PPAR alfa MeSH
• receptory adiponektinu MeSH
• receptory buněčného povrchu MeSH
• resistin MeSH
• triglyceridy MeSH