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PubMed2006

Adiponectin is a negative regulator of NK cell cytotoxicity.

NK cells are a key component of innate immune systems, and their activity is regulated by cytokines and hormones. Adiponectin, which is secreted from white adipose tissues, plays important roles in various diseases, including hypertension, cardiovascular diseases, inflammatory disorders, and cancer. In this study the effect of adiponectin on NK cell activity was investigated. Adiponectin was found to suppress the IL-2-enhanced cytotoxic activity of NK cells without affecting basal NK cell cytotoxicity and to inhibit IL-2-induced NF-kappaB activation via activation of the AMP-activated protein kinase, indicating that it suppresses IL-2-enhanced NK cell cytotoxicity through the AMP-activated protein kinase-mediated inhibition of NF-kappaB activation. IFN-gamma enhances NK cell cytotoxicity by causing an increase in the levels of expression of TRAIL and Fas ligand. The production of IFN-gamma, one of the NF-kappaB target genes in NK cells, was also found to be suppressed by adiponectin, accompanied by the subsequent down-regulation of IFN-gamma-inducible TRAIL and Fas ligand expression. These results clearly demonstrate that adiponectin is a potent negative regulator of IL-2-induced NK cell activation and thus may act as an in vivo regulator of anti-inflammatory functions.

Adiponectin↗
PubMed2003

[Research advancement of adipocytokine adiponectin].

The Adiponectin, an adipocytokine, is a plasma protein produced and secreted exclusively by adipose tissues. Adiponectin has important effects on angiocardiopathy, obesity and type 2 diabetes. In addition, adiponectin has certain roles in inflammation and hematopoiesis. Primarily results from adiponectin treatment of type 2 diabetes and some metabolism diseases suggest that adiponectin may serve as a potential and novel medicine.

Adipocytes↗
PubMed2005

[Serum concentrations of adiponectin in patients with restrictive and purgative subtype of mental anorexia].

BACKGROUND: The aim of our study was to compare serum concentrations of adiponectin, leptin and other selected parameters in female patients with restrictive subtype of anorexia nervosa (n=15), (RMA), binge/purge subtype of anorexia nervosa (n=11) (PMA) with age-matched healthy females, (C, n=14). METHODS AND RESULTS: RMA patients had the most severely decreased body mass index (BMI) and serum leptin levels of the three groups studied. These parameters were also significantly lower in PMA relative to C group. (BMI: RMA 14.61 +/- 0.49 kg/m2, PMA 17.30 +/- 0.25 kg/m2, C 23.21 +/- 0.96 kg/m2; leptin: RMA 1.39 +/- 0.31 ng/ml, PMA 3.72 +/- 0.77 ng/ml, C 9.17 +/- 1.53 ng/ml). In contrast, serum adiponectin levels were markedly increased in RMA patients (57.28 +/- 4.86 ug/ml) relative to other groups (PMA 40,25 +/- 2.18 microg/ml, K 26.84 +/- 2.40 microg/ml). Serum leptin levels positively correlated with BMI in all groups studied (r = 0.56, p = 0.002), while the inverse relationship was found for adiponectin levels and BMI (r = -0.72, p = 0.000003). The hormonal concentrations were measured by commercially available RIA and ELISA kits. CONCLUSIONS: The most significant changes of serum adiponectin and leptin levels were found in the RMA group with most severely decreased BMI and body fat content relative to rest of the groups. Possible role of increased adiponectin levels in the etiopathogenesis and/or metabolic changes in patients with anorexia nervosa is under the scope of our current investigations.

Adiponectin↗
PubMed2005

[Inflammatory markers and adiponectin plasma level in patients with type 2 diabetes].

INTRODUCTION: In patients with carbohydrate or lipid disturbances higher inflammatory markers levels and lower adiponectin levels were observed. These observations suggest the potential role of those markers in the pathogenesis of diabetes, obesity and atherosclerosis. INVESTIGATED GROUP AND METHODS: 25 type 2 diabetic patients (group A) and 15 patients without diabetes (group B) were included into the study. Glycated haemoglobin (HbAlc), total cholesterol and triglycerides, interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha) and adiponectin levels were measured in blood samples. Fasting plasma glucose and fasting plasma insulin were measured to calculate index of insulin resistance (homeostasis model assessment--IR/HOMA-IR/). RESULTS: Mean adiponectin level was significantly lower in patients with type 2 diabetes than in control patients (7,4 microg/ml vs 12,3 microg/ml; p<0,05). Blood levels of fasting insulin, IL-6, TNFalpha and HOMA-IR index were higher in people with diabetes than in control subjects but the differences were not statistically significant. No significant correlations were observed between adiponectin and inflammatory markers level and total cholesterol, triglyceride, HOMA-IR level and blood pressure. CONCLUSIONS: The findings indicate that adiponectin level is lower in patients with type 2 diabetes. We did not manage to confirm significantly elevated inflammatory markers levels in this group of patients.

Adiponectin↗
PubMed2006

Associations between hypertriglyceridemia and serum ghrelin, adiponectin, and IL-18 levels in HIV-infected patients.

HIV-related metabolic abnormalities include hypertriglyceridemia, hypercholesterolemia, insulin resistance, and diabetes mellitus. Recent studies suggest a role of ghrelin in promoting the deposition of triglycerides (TG) in the liver and regulating the metabolic action of adiponectin. Visceral fat is a key regulator of inflammation and it secretes proinflammatory cytokines (eg, interleukin-18, IL-18), with potential atherogenic activity. The aim of this study was to assay serum concentrations of ghrelin, adiponectin, and IL-18 in HIV+ patients, with and without hypertriglyceridemia, who were receiving highly active antiretroviral therapy (HAART). The 49 HIV+ patients were divided in 2 groups: 17 patients with serum TG concentration >200 mg/dl (group A) and 32 patients with normal serum TG concentration (group B). All subjects underwent viral and immunological evaluations and determinations of serum cholesterol, glucose, ghrelin, adiponectin, and IL-18. No differences of viral and immunological parameters were observed between the 2 groups. Serum levels of ghrelin were 768 +/- 596 pg/dl in group A and 470 +/- 248 pg/dl in group B (p = 0.01). Group A had lower serum adiponectin levels (8.4 +/- 3.6 microg/dl) than group B (18.2 +/- 10.1 microg/dl; p = 0.0001). Serum IL-18 levels were 455 +/- 199 pg/ml in group A and 258 +/- 233 pg/ml in group B (p = 0.005). The patients with hypertriglyceridemia showed a positive correlation between serum triglyceride and ghrelin levels (r = 0.51, p = 0.03). These findings suggest potential roles of ghrelin, adiponectin, and IL-18 in the pathogenesis of metabolic disorders in HIV-infected patients.

Adiponectin↗
PubMed2006

[Study on the relationship between serum adiponectin and insulin resistance in women with polycystic ovary syndrome].

OBJECTIVE: To study the relationship between serum adiponectin and insulin resistance in women with polycystic ovary syndrome (PCOS). METHODS: Forty women with PCOS and twenty five healthy women were divided into PCOS obese group [body weight index (BMI) > or = 25kg/m(2)], PCOS non-obese group (BMI < 25 kg/m(2)) and control group. There are 19 cases in PCOS obese group and 21 cases in PCOS non-obese group, 9 cases in obese control group and 16 in non-obese control group. Serum adiponectin levels of the four groups were detected by enzyme linked immunosorbent assay (ELISA) method, insulin by electrochemiluminescence immunoassay method, blood sugar by glucose oxidation enzyme method, tumor necrosis factor-alpha (TNF-alpha) by radioimmunoassay. Insulin sensitivity index (ISI) was calculated. RESULTS: (1) Serum adiponectin levels of PCOS obese group was (1.6 +/- 0.5) mg/L, of PCOS non-obese group was (3.0 +/- 0.6) mg/L. Their values were lower than obese control group (3.2 +/- 0.3) mg/L, and non-obese control group (4.9 +/- 0.5) mg/L (P < 0.05). (2) Fasting insulin levels of PCOS obese group was (17 +/- 6) mU/L, PCOS non-obese group was (14 +/- 6) mU/L. They were higher than obese control group (10 +/- 3) mU/L, and non-obese control group (7 +/- 3) mU/L (P < 0.05). (3) Fasting blood sugar level was (5.2 +/- 0.7) mmol/L in PCOS obese group, in PCOS non-obese group was (5.1 +/- 0.6) mmol/L, in obese control group was (5.4 +/- 0.5) mmol/L, and non-obese control group (4.8 +/- 0.6) mmol/L, without marked difference among four groups. (4) TNF-alpha levels of PCOS obese group was (1.32 +/- 0.14) microg/L, of PCOS non-obese group was (1.02 +/- 0.12) microg/L. They were higher than obese control group (0.93 +/- 0.15) microg/L, and non-obese control group (0.63 +/- 0.18) microg/L (P < 0.05). (5) ISI of PCOS obese group was -4.5 +/- 0.3, PCOS non-obese group was -4.1 +/- 0.4. Their values were lower than obese control group -3.6 +/- 0.3, and non-obese control group (-3.1 +/- 0.4) (P < 0.05). Serum adiponectin levels of the women with PCOS were correlated negatively with BMI (r = -0.56, P < 0.05), and correlated positively with ISI (r = 0.49, P < 0.05). CONCLUSION: Serum adiponectin levels of women with PCOS is decreased compared with healthy women, particularly in obese women with PCOS. The decrease is correlated with ISI.

Adiponectin↗
PubMed2006

[Blood adiponectin and leptin levels in menopausal metabolic syndrome].

The aim of our investigation was the study of blood adiponectin and leptin levels in patients with menopausal metabolic syndrome (MMS) and their correlation with the parameters of MMS features. 40 females with menopause have been investigated. In 38 cases diabetes mellitus type 2 has been registered, and in 2 - impaired glucose tolerance. Mean duration of postmenopausal period was 11,1+/-7,4. Control group consisted of 10 females of postmenopausal age. The blood content of adiponectin and leptin was measured by ELISA. For MMS diagnostics WHO classification (2002) was applied. In basic group MMS was revealed in 37 patients, in control group - in 3 cases (chi(2)=19,53, p<0,001). It was not observed significant difference in blood adiponectin levels of basic and control groups (16,4+/-7,6 vs. 16,3+/-6,1, p=NS), but blood leptin level was significantly higher in study group in comparison with controls (166,7+105,3 vs. 60,3+/-51,0, p<0,001). Significant correlations of blood adiponectin and leptin levels with the parameters of MMS features were observed. Obtained results show that blood adiponectin level in MMS does not differ from the values in control group, although blood leptin level is significantly higher than the one among controls. They significantly correlated with the parameters of MMS features.

Adiponectin↗
PubMed2006

[The role of adiponectin in atherosclerosis].

Adiponectin is a adipose tissue-derived protein. In the light of current investigations, the role of adiponectin goes far beyond only adipose tissue regulatory factor, being involved in some pathological processes as endothelium damage or atherosclerosis. Unique properties of adiponectin make it a very promising agent that posses ability to slow down the progression of atherosclerosis. In this article, a structure and a function of adiponectin have been reviewed. The special emphasis was put upon the role of adiponectin in atherosclerosis.

Adiponectin↗
PubMed2006

[Polymorphisms of adiponectin and resistin genes in patients with obesity and anorexia nervosa].

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.

Adiponectin↗
PubMedDate not supplied

Fasting insulin, adiponectin, hs-CRP levels, and the components of metabolic syndrome.

AIM: in this study we report the relationship between fasting plasma insulin, C-reactive protein, adiponectin levels and the components of metabolic syndrome. METHODS: for the diagnosis of metabolic syndrome we used the modified NCEP ATP criteria for Asian people. Complete routine physical examinations were performed to all subjects including blood pressure, waist circumference. After 12-hours fasting, blood sample was taken for fasting plasma glucose, fasting insulin, and lipid profiles. Fasting insulin was determined by RIA, adiponectin by ELISA, and hs-CRP by sensitive immunometric assay. According to NCEP ATP III, the metabolic syndrome consists of five components. Subjects fulfilling the studied criteria were divided into five groups according to the component/components they had. RESULTS: during the study, 118 adult individuals can be covered, including 88 patients (68,8%) with metabolic syndrome. They consist of 19 subjects who had only 1 component, 21 subjects had 2 components, 31 subjects with 3 components, 34 subjects with 4 components, and 23 subjects had 5 component. All subjects were overweight/obese (BMI > 23 kg/m), but patients with metabolic syndrome were significantly more obese compared to the non-metabolic syndrome (p < 0.05). There was no significant difference in age among all individuals. Fasting insulin, hs-CRP levels is increasing with the increasing number of components of metabolic syndrome, being higher among those with 3-5 components, while adiponectin is decreasing with the number of the components. Fasting insulin 3,5+1,1 uU/ml, 3,6+1,4 uU/ml, 5,9+1,8 uU/ml, 7,8+2,1 uU/ml, 7,9+2,3 uU/ml respectively, hs-CRP 2,8+1,2 mg/L, 5.6+3.4 mg/L, 7.4+4.4 mg/L, 9.0+4.7 mg/L, 9.5+3,9 mg/L, and adiponectin 9.1+3.5 ng/ml, 8.6+1.6 ng/ml, 3.4+1.2 ng/ml, 3.2+1.3 ng/ml, 2.8+0.9 ng/ml in 3,4,5 components respectively. CONCLUSION: there is a relationship between the number of components of metabolic syndrome and the increasing levels of fasting insulin, and hs-CRP, and low levels of adiponectin. These may explain in part the risk of cardiovascular events among individuals with metabolic syndrome.

Adiponectin↗
PubMed2005

Fasting serum levels of adiponectin, ghrelin, and leptin in men with spinal cord injury.

OBJECTIVES: To measure serum levels of adiponectin, ghrelin, and leptin in men with spinal cord injury (SCI) and to investigate possible correlations between these serum levels and various factors, such as body mass index (BMI), age, injury level, and duration of injury. DESIGN: Cross-sectional. SETTING: A university hospital that is a tertiary referral center. PARTICIPANTS: Eighty-nine men with traumatic neurologically complete SCI (30 with tetraplegia, 59 with paraplegia) and 37 age- and BMI-matched male controls. Subjects with SCI were injured at the mean age +/- standard error of 28.5+/-1.0 years (range, 14.7-59.1 y) and the mean injury duration was 10.8+/-0.7 years (range, 1.1-27.7 y). INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Serum levels of adiponectin, ghrelin, and leptin and BMI. RESULTS: Serum leptin levels in subjects with SCI (mean, 7.0+/-0.5 mg/mL) [corrected] were significantly higher than those in able-bodied controls (mean, 4.7+/-0.6 mg/mL) [corrected] (P<.01). The group with tetraplegia had higher serum leptin levels than the group with paraplegia, but this did not reach a statistically significant level (8.2+/-1.1 ng/mL vs 6.4+/-0.5 mg/mL [corrected] P=.097). There were significant differences in serum leptin levels among the 3 groups by 1-way analysis of variance (P=.008). Serum adiponectin levels in subjects with SCI (7.1+/-0.5 mg/mL) [corrected] were higher than those in able-bodied controls (5.6+/-0.5 mg/mL) [corrected] but this was not statistically significant (P=.08). In contrast, serum levels of ghrelin in subjects with SCI (302.0+/-17.5 pg/mL) were similar to those in the controls (264.0+/-27.0 pg/mL) (P=.24). Serum leptin levels correlated positively with BMI (SCI, r=.698, P<.001; controls, r=.782, P<.001), whereas serum adiponectin (SCI, r=-.527, P<.001; controls, r=-.315, P=.057) and ghrelin (SCI, r=-.368, P<.001; controls, r=-.447, P=.006) levels correlated negatively with the BMI in both subjects with SCI and controls. CONCLUSIONS: Men with SCI have significantly higher serum leptin levels than able-bodied controls, and serum leptin levels correlated with the degree of neurologic deficit. Men with SCI had a tendency toward higher serum adiponectin level than able-bodied controls. Serum levels of ghrelin in men with SCI were similar to those of controls.

Adult↗
PubMed2005

Pharmacological PPARgamma stimulation in contrast to beta cell stimulation results in an improvement in adiponectin and proinsulin intact levels and reduces intima media thickness in patients with type 2 diabetes.

The role of intact proinsulin and adiponectin in endothelial dysfunction and insulin resistance has been receiving increasing attention. This study investigates the effect of PPARgamma stimulation or beta-cell stimulation on metabolic and vascular parameters in patients with type 2 diabetes. In our study, 173 type 2 diabetic patients were recruited and randomly assigned to pioglitazone 45 mg or glimepiride 1 - 6 mg treatment. Intima media thickness of the carotid artery, glycemic control, insulin resistance, adiponectin and intact proinsulin levels were assessed at baseline and after six months of treatment. Despite similar improvements in metabolic control (HbA (1c) after 24 weeks: - 0.8 +/- 0.9% [pioglitazone] vs. - 0.6 +/- 0.8% [glimepiride]; mean +/- SD; p < 0.0001, respectively), improvements in intima media thickness (- 0.033 +/- 0.052 mm; p < 0.0001), proinsulin intact (- 5.92 +/- 10.04 pmol/l; p < 0.0001), adiponectin (10.9 +/- 6.3 microg/ml; p < 0.0001) and HOMA score (- 2.21 +/- 3.40; p < 0.0001) were observed by pioglitazone but not glimepiride treatment. Reduction in intima media thickness was correlated with improved insulin sensitivity (r = 0.29; p = 0.0003), and proinsulin intact levels (r = 0.22; p = 0.006), while an inverse correlation was found with adiponectin levels (r = - 0.37; p < 0.0001). Measurement of adiponectin and intact proinsulin enables characterization of the metabolic situation and an estimation of atherosclerotic risk in patients with type 2 diabetes.

Aged↗
PubMed2005

Adiponectin and its potential in the treatment of obesity, diabetes and insulin resistance.

Adiponectin is a protein hormone produced exclusively by adipocytes. Its circulating levels are decreased in individuals with obesity, atherosclerosis and insulin resistance, suggesting that its deficiency may have a causal role in the etiopathogenesis of these diseases. Studies have shown that adiponectin administration in rodents has insulin-sensitizing, anti-atherogenic and anti-inflammatory effects and under certain settings also decreases body weight. Therefore, adiponectin replacement in humans may represent a promising approach to prevent and/or treat obesity, insulin resistance and type 2 diabetes; however, clinical studies with adiponectin administration need to be conducted to confirm this hypothesis. Current experimental and clinical data regarding adiponectin physiology and pathophysiology are detailed in this review.

Diabetes Mellitus, Type 2↗
PubMed2005

Expression profiles of adiponectin receptors in mouse embryos.

Adiponectin is a protein secreted from adipocytes and it plays an important endocrine role in glucose and lipid homeostasis. A reverse correlation between plasma adiponectin concentrations and insulin resistance has been established in both animals and humans. Adiponectin exerts its function by interacting with membrane receptors, including AdipoR1 and AdipoR2. We investigated the expression pattern of these two adiponectin receptors in mouse embryos. At stages E12.5 and E15.5, both AdipoR1 and AdipoR2 are highly expressed in the nervous system including the trigeminal ganglion, glossopharyngeal ganglion and dorsal root ganglia. AdipoR1 is highly expressed in many tissues derived from primitive gut, including the lung, liver, pancreas and small intestines. Generally, the expression level of AdipoR2 is weaker and more restricted than AdipoR1 in most of the tissues. In addition, AdipoR1 expression can be found in heart, vertebrate, developing bones and cartilage, and many other tissues. This study reveals that AdipoR1 and AdipoR2 have differential but overlapping expression profiles during mouse development.

Adiponectin↗
PubMed2006

The potential of adiponectin in driving arthritis.

Articular adipose tissue is a ubiquitous component of human joints, but its local functions are largely unknown. Because recent studies revealed several links between adipose tissue, adipocytokines, and arthritis, we investigated the expression of the adipocytokine adiponectin and its functional role in articular adipose tissue and synovium of patients with different arthritides. In contrast to its protective role in endocrinological and vascular diseases, adiponectin was found to be involved in key pathways of inflammation and matrix degradation in the human joint. The effects of adiponectin in human synovial fibroblasts appear to be highly selective by inducing only two of the main mediators of rheumatoid arthritis pathophysiology, IL-6 and matrix metalloproteinase-1, via the p38 MAPK pathway. Owing to the observation that these effects could be inhibited by different TNF-alpha inhibitors, adipocytokines such as adiponectin may also be key targets for therapeutic strategies in inflammatory joint diseases. In summary, articular adipose tissue and adipocytokines cannot be regarded as innocent bystanders any more in chronic inflammatory diseases such as arthritis.

Adalimumab↗
PubMed2004

Serum concentrations of adiponectin and leptin in patients with thyroid dysfunctions.

Thyroid dysfunction is associated with metabolic changes that affect mass and adipocyte function, as well as lipid and carbohydrate metabolism. Adipose tissue performs complex metabolic and endocrine functions. Leptin and adiponectin are two of the most important adipocytokines, both involved in the regulation of intermediate metabolism. The aim of this study was to evaluate the relationships between thyroid status and circulating levels of the two adipose tissue hormones. We studied 15 patients with hyperthyroidism, 15 patients with hypothyroidism and 15 euthyroid subjects, all matched by sex, age and body mass index (BMI). Serum concentrations of free thyroxine, free tri-iodothyronine, thyrotropin, leptin and adiponectin and anthropometric parameters (weight, height, BMI) were assessed. No significant difference was found among the 3 groups, as assessed by Student's t-test, both for adiponectin and leptin. We conclude that metabolic changes associated with thyroid dysfunction are not related to variations in serum levels of adiponectin or leptin.

Adiponectin↗
PubMed2003

Allele-specific differential expression of a common adiponectin gene polymorphism related to obesity.

Adiponectin gene polymorphisms have recently been reported to be associated with obesity, insulin sensitivity, and the risk of type 2 diabetes. We examined a T94G polymorphism of the adiponectin gene in 245 ostensibly normal nondiabetic subjects. The G allele frequency was lower among subjects with higher BMI (> or =27) than in those with lower BMI. BMI was inversely correlated with the dose of G allele. Multivariate linear regression analyses showed that the adiponectin genotypes were significantly related to BMI after adjusting for age and gender. The dose of the G allele was associated with a reduction of approximately 1.12 kg/m(2) in BMI. We further found that the relative mRNA levels of G allele were consistently higher than those of T allele in the omental adipose tissue from 21 heterozygous subjects. Finally, we observed that the expression levels of adiponectin affected insulin-stimulated glucose uptake in differentiated 3T3-L1 adipocytes. In conclusion, the allele-specific differential expression of this common polymorphism could be responsible for its biological effects observed in this and the other studies.

3T3-L1 Cells↗
PubMed2005

Adiponectin and human pregnancy.

Adiponectin is an adipose tissue-derived plasma protein that is involved in regulation of insulin resistance and glucose hemostasis. Human pregnancy is characterized by an increase in insulin resistance. Therefore, it is only natural that the role of adiponectin, a modulator of insulin resistance, is subject to investigation during gestation. Furthermore, conditions associated with increased insulin resistance, such as gestational diabetes and preeclampsia, may be influenced by this hormone. Adiponectin, a key modulator of insulin action and glucose metabolism, both known to regulate fetal growth, is a plausible candidate for regulation of intrauterine fetal development. In this review, we summarize the recent studies describing the relationship between adiponectin, pregnancy, and fetal growth.

Adiponectin↗