Adiponectin mRNA Levels in Parametrial Adipose Tissue and Serum Adiponectin Levels are Reduced in Mice During Late Pregnancy

Kondo, Eiji; Sugiyama, Takashi; Kusaka, Hideto; Toyoda, Nagayasu

doi:10.1055/s-2004-825726

Cited by 20 publications

(13 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The use of Gonal-F raised estradiol levels signifi cantly, and in line with previous reports on the effect of estradiol [10,11] , we observed a decrease in serum adiponectin levels from Day-basal to Day-hCG ( fi g. 1 ). It has been suggested that estradiol has a direct negative impact on serum adiponectin levels in vivo [11] .…”

Section: Discussionsupporting

confidence: 77%

See 1 more Smart Citation

Serum Adiponectin Levels Increase after Human Chorionic Gonadotropin Treatment during in vitro Fertilization

Liu

Tsai²,

Chen³

et al. 2006

Gynecol Obstet Invest

View full text Add to dashboard Cite

Aims: To determine whether or not serum adiponectin concentrations are influenced by ovarian hyperstimulation during in vitro fertilization (IVF). Methods: This study involved 52 women who were participating in IVF-ET cycles. Adiponectin levels in serum were determined by radioimmunoassay and compared. Results: Serum adiponectin levels fell from Day-basal to Day-hCG (p = 0.047), and then rose on Day-OR and again on Day-7ET (p < 0.001; p < 0.001). Estradiol levels on Day-hCG were significantly and positively correlated with serum adiponectin levels on Day-OR and Day-7ET (r = 0.325, p = 0.019; r = 0.372, p = 0.007). Progesterone levels on Day-OR positively correlated with serum adiponectin levels on Day-basal (r = 0.278, p = 0.046). There was also a positive correlation between progesterone levels on Day-7ET and serum adiponectin levels on Day-OR (r = 0.289, p = 0.038). Multiple linear regression analysis revealed that adiponectin levels on Day-OR and Day-7ET were negatively correlated with age and body mass index after adjustment was made for concomitant diseases. Conclusions: To sum up, following gonadotropin treatment, serum adiponectin levels decrease as a result of the negative effect of high estradiol levels on adiponectin production. Conversely, serum adiponectin levels increase following human chorionic gonadotropin treatment.

show abstract

Section: Discussionsupporting

confidence: 77%

“…The administration of insulin-sensitizing drugs signifi cantly increases serum adiponectin levels in insulin-resistant humans [9] . Adiponectin mRNA and serum adiponectin concentrations are signifi cantly reduced at pregnancy [10] . It has been suggested that estradiol has a direct negative impact on serum adiponectin levels in vivo [11] .…”

Section: Introductionmentioning

confidence: 99%

Serum Adiponectin Levels Increase after Human Chorionic Gonadotropin Treatment during in vitro Fertilization

Liu

Tsai²,

Chen³

et al. 2006

Gynecol Obstet Invest

View full text Add to dashboard Cite

show abstract

“…Our longitudinal analysis in women from the pregravid state to the third trimester indicates that pregnancy in humans is a physiological situation in which circulating adiponectin is decreased, as is found in mice [11,27]. The 25% increase in fat mass from pregravid state to late pregnancy, together with the negative correlation between circulating adiponectin concentrations and fat mass, suggests that adipose tissue accretion is associated with signals for lowering adiponectin production or secretion even in the absence of obesity.…”

Section: Pregnancy Is a Situation Of Hypoadiponectinaemiasupporting

confidence: 56%

Adiponectin in human pregnancy: implications for regulation of glucose and lipid metabolism

et al. 2006

View full text Add to dashboard Cite

Aims/hypothesis: Adiponectin is upregulated during adipogenesis and downregulated in insulin-resistant states. The mechanism(s) governing the re-arrangements from adipogenesis to facilitated lipolysis during pregnancy are unknown. Our purpose was to analyse the role of adiponectin relative to the metabolic changes in human pregnancy. Subjects, materials and methods: Lean women (BMI <25 kg/m²) were evaluated longitudinally before conception, and in early (12-14 weeks) and late (34-36 weeks) pregnancy. Insulin sensitivity was measured using the glucose clamp technique. Venous blood and subcutaneous adipose tissue biopsies were obtained at each time point. Results: Adiponectin concentrations were lower in the third trimester than in the pregravid condition (9.9±1.4 vs 13.5±1.8 μg/ml). The hypoadiponectinaemia was reflected by a 2.5-fold decrease in white adipose tissue adiponectin mRNA. These changes were associated with a 25% increase in fat mass (23.7±2.9 vs 18.9±2.9 kg). Insulin infusion decreased high molecular weight adiponectin complexes in pregravid women (9.9±0.6 vs 6.2±0.06) and the suppressive effect of insulin was lost during pregnancy. The pregnancy-mediated changes in adiponectin were strongly correlated with basal insulin levels and insulin sensitivity (p<0.0001). The relationship between adiponectin and insulin sensitivity was related to the decreased insulin regulation of glucose utilisation (r=0.55, p<0.001) but not of endogenous hepatic glucose production. Conclusions/interpretation: These data demonstrate that pregnancy is associated with adiponectin changes in lean women. Hypoadiponectinaemia is reflected by a lower amount of high molecular weight adiponectin and by the ratio of high to low molecular weight multimers. The adiponectin changes relate to decreased insulin sensitivity of glucose disposal rather than alterations of lipid metabolism.

show abstract

“…Consistent with these observations, only mice lacking iNOS, which showed a marked elevation in plasma high-molecular weight adiponectin levels, exhibited improved glucose tolerance and liver insulin action in response to rosiglitazone, confirming the high sensitivity of the liver to changes in highmolecular weight form concentrations (7). Adipose tissue remodeling caused by rosiglitazone treatment of iNOS knockout mice likely explains the raised plasma highmolecular weight adiponectin complexes in these animals because previous studies reported a strong inverse relationship between adipose cell size and adiponectin secretion (52,53).…”

Section: Discussionmentioning

confidence: 61%

Obese Mice Lacking Inducible Nitric Oxide Synthase Are Sensitized to the Metabolic Actions of Peroxisome Proliferator–Activated Receptor-γ Agonism

et al. 2008

View full text Add to dashboard Cite

OBJECTIVE-Synthetic ligands for peroxisome proliferatoractivated receptor-␥ (PPAR-␥) improve insulin sensitivity in obesity, but it is still unclear whether inflammatory signals modulate their metabolic actions. In this study, we tested whether targeted disruption of inducible nitric oxide (NO) synthase (iNOS), a key inflammatory mediator in obesity, modulates the metabolic effects of rosiglitazone in obese mice. RESEARCH DESIGN AND METHODS-iNOSϪ/Ϫ and iNOS ϩ/ϩ were subjected to a high-fat diet or standard diet for 18 weeks and were then treated with rosiglitazone for 2 weeks. Whole-body insulin sensitivity and glucose tolerance were determined and metabolic tissues harvested to assess activation of insulin and AMP-activated protein kinase (AMPK) signaling pathways and the levels of inflammatory mediators.RESULTS-Rosiglitazone was found to similarly improve whole-body insulin sensitivity and insulin signaling to Akt/PKB in skeletal muscle of obese iNOS Ϫ/Ϫ and obese iNOS ϩ/ϩ mice. However, rosiglitazone further improved glucose tolerance and liver insulin signaling only in obese mice lacking iNOS. This genotype-specific effect of rosiglitazone on glucose tolerance was linked to a markedly increased ability of the drug to raise plasma adiponectin levels. Accordingly, rosiglitazone increased AMPK activation in muscle and liver only in obese iNOS Ϫ/Ϫ mice. PPAR-␥ transcriptional activity was increased in adipose tissue of iNOS Ϫ/Ϫ mice. Conversely, treatment of 3T3-L1 adipocytes with a NO donor blunted PPAR-␥ activity. CONCLUSIONS-Our results identify the iNOS/NO pathway as a critical modulator of PPAR-␥ activation and circulating adiponectin levels and show that invalidation of this key inflammatory mediator improves the efficacy of PPAR-␥ agonism in an animal model of obesity and insulin resistance.

show abstract

Adiponectin mRNA Levels in Parametrial Adipose Tissue and Serum Adiponectin Levels are Reduced in Mice During Late Pregnancy

Cited by 20 publications

References 20 publications

Serum Adiponectin Levels Increase after Human Chorionic Gonadotropin Treatment during in vitro Fertilization

Serum Adiponectin Levels Increase after Human Chorionic Gonadotropin Treatment during in vitro Fertilization

Adiponectin in human pregnancy: implications for regulation of glucose and lipid metabolism

Obese Mice Lacking Inducible Nitric Oxide Synthase Are Sensitized to the Metabolic Actions of Peroxisome Proliferator–Activated Receptor-γ Agonism

Contact Info

Product

Resources

About