Gestational Diabetes is Associated with Depressed Adiponectin Levels

Thyfault, John P.; Hedberg, Elizabeth M.; Anchan, Raymond M.; Thorne, Olga P.; Isler, Christy; Newton, Edward R.; Dohm, G. Lynis; DeVente, James

doi:10.1016/j.jsgi.2004.07.003

Cited by 56 publications

(50 citation statements)

References 22 publications

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“…Non-Caucasians had lower adiponectin levels than Caucasians. Significantly lower differences were still found between non-Caucasian subjects when grouped [33,35]. Other studies had examined adiponectin in GDM and healthy pregnants.…”

Section: Discussionmentioning

confidence: 86%

Maternal Leptin, Adiponectin, Resistin, Visfatin and Tumor Necrosis Factor-Alpha in Normal and Gestational Diabetes

Noureldeen

Qusti²,

Al‐Seeni³

et al. 2013

Ind J Clin Biochem

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Gestational diabetes mellitus (GDM) is a common medical complication associated with pregnancy. The present study evaluates the changes in maternal adipocytokines (leptin, adiponectin, resistin, visfatin and tumor necrosis factor-alpha; TNF-a) in pregnancy complicated with GDM compared to normal pregnancy at 2nd and 3rd trimesters. The study included total number of 142 pregnant women classified into 4 groups: normal pregnancy (n = 33) and pregnancy with GDM (n = 24) both at 2nd trimester and normal pregnancy (n = 38) and GDM (n = 47) at 3rd trimester. Both GDM groups were significantly presented with elevated body mass index, fasting blood sugar and abnormal oral glucose tolerance test compared to their matched control. Results indicated reduction in maternal serum leptin and adiponectin in GDM compared to normal pregnancy at 3rd trimester. Elevated resistin and TNF-a were evident among pregnancy complicated with GDM at both tested trimesters. On the other hand, significant elevation in maternal visfatin was noted between GDM and matched control at 2nd trimester only. Significant increase in maternal leptin and visfatin and resistin was noted by advances in gestational period in healthy pregnancy. On the other hand, reduced adiponectin and elevated visfatin mean values were noticed in GDM at 3rd compared to 2nd trimester. It could be concluded that increased insulin resistance accompanies GDM is associated with suppressed leptin and adiponectin and increased resistin and TNF-a which might suggest their involvement in the development of GDM.

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Section: Discussionmentioning

confidence: 86%

Maternal Leptin, Adiponectin, Resistin, Visfatin and Tumor Necrosis Factor-Alpha in Normal and Gestational Diabetes

Noureldeen

Qusti²,

Al‐Seeni³

et al. 2013

Ind J Clin Biochem

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“…65 This pattern is reversed in late pregnancy, as pre-eclampsia is associated with hyperadiponectinemia. 66 Other studies report that hypoadiponectinemia and preeclampsia correlate only when obesity 63 and gestational diabetes 67 are present as complicating factors.…”

Section: Effects Of Adiponectin On Reproduction and Fertilitymentioning

confidence: 99%

The ‘beneficial’ adipokines in reproduction and fertility

et al. 2007

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The objective of this study was to review the available information on the signaling proteins produced by adipose tissue in the context of their role in regulating reproductive processes, including ovarian and uterine function. It is well known that both obesity and excessive leanness are associated with reproductive dysfunction. Adipokines are cytokines predominately or exclusively expressed by adipose tissue that circulate and affect target tissues. Four known adipokines, adiponectin, visfatin/ PBEF, omentin and vaspin, all increase tissue sensitivity to insulin, and are thus described as 'beneficial'. There is strong support for a role for adiponectin in the function of the ovary and placenta. There is evidence for direct effects of this adipokine on the late stages of folliculogenesis, and additive interactions of adiponectin with insulin and gonadotropins in inducing periovulatory changes in ovarian follicles. In addition, clinical and genomic studies associate hypoadiponectinemia with obesity-related reproductive disorders, including the polycystic ovarian syndrome. The roles for visfatin/PBEF, omentin and vaspin in reproduction remain to be established. The conclusion thus drawn is that the expression of insulin-sensitizing adipokines varies with adipose abundance. These adipokines have demonstrated both the potential effects on ovarian function and the possible effects on the formation of the placenta, acting through multiple mechanisms.

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“…Data from additional gravid patients from the same clinic were added for statistical analysis examining the relationship between BMI and HOMA, by subject group and by BMI categorization. Correlation of BMI and HOMA in healthy, control patients did not show a significant relationship for all BMI categories of overweight patients (BMI: 25-40+), however patients within the "normal" BMI range (20)(21)(22)(23)(24)(25) demonstrated an inverse correlation with HOMA (r= -0.055, p=0.011). Due to the extensive research on relationship between obesity doi: 10.7243/2050-0866-2-23 and diabetes, one would expect a positive correlation between BMI and HOMA in both non-pregnant subjects [31][32][33] and in pregnant subjects [34,35].…”

Section: Resultsmentioning

confidence: 80%

“…One such endocrine response is the low levels of adiponectin that were measured in these same patients [20], proposing a potential regulatory function for adiponectin on NPY concentrations independent of the leptin feedback. Adiponectin has previously been shown modulate other adiposity-and reproductionrelated hormones including inhibit luteinizing hormone (LH) and gonadotropin-releasing hormone (GnRH) [44,45] and affect insulin sensitivity [1].…”

Section: Doi: 107243/2050-0866-2-23mentioning

confidence: 92%

“…Accordingly, increased leptin levels concurrent with hyperphagia suggest the development of leptin resistance during pregnancy in addition to insulin resistance [2,19], leading us to investigate differential peripartum levels of this peptide as well. Other regulatory peptides of interest include ghrelin, tumor necrosis factoralpha (TNF-α), and previously reported adiponectin [20], which all contribute to energy balance, metabolism and insulin resistance through various pathways [21][22][23]. Recently, TNF-α production has been demonstrated in adipose tissue and when, interacting with the hypothalamus, may also affect appetite.…”

Section: Introductionmentioning

confidence: 99%

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Peripartum changes in the orexigenic CNS peptide neuropeptide-Y in gestational diabetics

Anchan

Lindsey²,

Newton³

et al. 2013

J Diab Res Clin Met

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Background: Development of relative insulin resistance during pregnancy is a normal physiologic change related to placental lactogen and pregnancy-associated elevated lipid concentrations. Several studies have investigated the role of tissue response, tyrosine kinase insulin receptor phosphorylation, and other cytokines that might contribute to development of such resistance. In this study, we specifically investigate the accompanying changes in concentrations of the orexigenic neurotransmitter neuropeptide Y (NPY) during pregnancy with the development and resolution of insulin resistance in gestational diabetics. Given that increased NPYergic activity is associated with increased eating behavior and body weight, we hypothesize levels of the central nervous system (CNS) peptide NPY will shift, along with other factors such as adiponectin, leptin, and ghrelin, in the development and resolution of gestational diabetes mellitus. Methods: Antepartum and postpartum plasma concentrations of NPY, leptin, ghrelin, tumor necrosis factor-alpha, glucose, and insulin were measured in gravid patients that were healthy (N=22), class A1 and A2 gestational diabetics (N=8), or type 2 diabetics (N=4). Homeostatic Model Assessment of insulin resistance was also calculated. Data was analyzed using a t-test and considered significant with p<0. 05. Results: We demonstrate that during the third trimester, class A2 gestational diabetics display an elevated NPY concentration. This elevated NPY begins to resolve immediately postpartum, normalizing by the patient's 6 week postpartum visit. The associated Homeostatic Model Assessment of insulin resistance index (HOMA) is consistent with these observations showing a concomitant elevation of HOMA intrapartum with improved insulin resistance within 24 hours postpartum. Discussion: Collectively, these results suggest a role for central nervous system involvement in the development of insulin resistance during gestational diabetes. Additionally, rising NPY levels during pregnancy may warrant routine patient surveillance for the development of occult insulin resistance and the obstetrical management of the same.

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Gestational Diabetes is Associated with Depressed Adiponectin Levels

Abstract: Class A2 and B gestational diabetes are associated with suppressed levels of adiponectin, similar to that found in other insulin-resistant states (type II diabetes and obesity).

Cited by 56 publications

References 22 publications

Maternal Leptin, Adiponectin, Resistin, Visfatin and Tumor Necrosis Factor-Alpha in Normal and Gestational Diabetes

Maternal Leptin, Adiponectin, Resistin, Visfatin and Tumor Necrosis Factor-Alpha in Normal and Gestational Diabetes

The ‘beneficial’ adipokines in reproduction and fertility

Peripartum changes in the orexigenic CNS peptide neuropeptide-Y in gestational diabetics

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