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

Catalano, Patrick M.; Hoegh, M.; Minium, Judi; Huston-Presley, Larraine; Bernard, Steven; Kalhan, Satish C.; Mouzon, Sylvie Hauguel-de

doi:10.1007/s00125-006-0264-x

Cited by 240 publications

(250 citation statements)

References 51 publications

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“…Circulating levels may also reflect the contribution of subcutaneous adipose tissue expression, which for some adipokines, such as leptin, is significantly greater in subcutaneous fat than in visceral fat (10). Surprisingly, serum levels of adiponectin were unchanged in the three groups studied, which is in contrast to human studies that found adiponectin levels to be decreased in late gestation (6). This difference may be due to the adiponectin expressed in the rodent placenta and perhaps a species-specific difference in the amount that reaches the maternal compartment.…”

Section: Discussioncontrasting

confidence: 65%

Accretion of visceral fat and hepatic insulin resistance in pregnant rats

Einstein

Fishman

Muzumdar

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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Insulin resistance (IR) is a hallmark of pregnancy. Because increased visceral fat (VF) is associated with IR in nonpregnant states, we reasoned that fat accretion might be important in the development of IR during pregnancy. To determine whether VF depots increase in pregnancy and whether VF contributes to IR, we studied three groups of 6-mo-old female Sprague-Dawley rats: 1) nonpregnant sham-operated rats (Nonpreg; n = 6), 2) pregnant sham-operated rats (Preg; n = 6), and 3) pregnant rats in which VF was surgically removed 1 mo before mating (PVF−; n = 6). VF doubled by day 19 of pregnancy (Nonpreg 5.1 ± 0.3, Preg 10.0 ± 1.0 g, P < 0.01), and PVF− had similar amounts of VF compared with Nonpreg (PVF− 4.6 ± 0.8 g). Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp in late gestation in chronically catheterized unstressed rats. Glucose IR (mg·kg−1·min−1) was highest in Nonpreg (19.4 ± 2.0), lowest in Preg (11.1 ± 1.4), and intermediate in PVF− (14.7 ± 0.6; P < 0.001 between all groups). During the clamp, Nonpreg had greater hepatic insulin sensitivity than Preg [hepatic glucose production (HGP): Nonpreg 4.5 ± 1.3, Preg 9.3 ± 0.5 mg·kg−1·min−1; P < 0.001]. With decreased VF, hepatic insulin sensitivity was similar to nonpregnant levels in PVF− (HGP 4.9 ± 0.8 mg·kg−1·min−1). Both pregnant groups had lower peripheral glucose uptake compared with Nonpreg. In parallel with hepatic insulin sensitivity, hepatic triglyceride content was increased in pregnancy (Nonpreg 1.9 ± 0.4 vs. Preg 3.2 ± 0.3 mg/g) and decreased with removal of VF (PVF− 1.3 ± 0.4 mg/g; P < 0.05). Accretion of visceral fat is an important component in the development of hepatic IR in pregnancy, and accumulation of hepatic triglycerides is a mechanism by which visceral fat may modulate insulin action in pregnancy.

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Section: Discussioncontrasting

confidence: 65%

Accretion of visceral fat and hepatic insulin resistance in pregnant rats

Einstein

Fishman

Muzumdar

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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“…Second, low adiponectin has been repeatedly associated with insulin resistance, consistent with the known insulin-sensitising bio-activity of the protein [8,11]. This inverse relationship between adiponectin and insulin resistance has also been consistently observed during pregnancy and in GDM [20,21,27]. Finally, a growing body of literature has recently queried a link between adiponectin and beta cell function, although conclusive resolution of this question remains elusive owing to some conflicting observations in this asyet modest literature.…”

Section: Discussionmentioning

confidence: 86%

Low adiponectin concentration during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia

Retnakaran

Qi²,

Connelly

et al. 2009

Diabetologia

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Aims/hypothesis The postpartum phase following gestational diabetes (GDM) is characterised by subtle metabolic defects, including the beta cell dysfunction that is believed to mediate the increased future risk of type 2 diabetes in this patient population. Low circulating levels of adiponectin and increased leptin and C-reactive protein (CRP) have recently emerged as novel diabetic risk factors, although their relevance to GDM and subsequent diabetes has not been characterised. Thus, we sought to determine whether adiponectin, leptin and CRP levels during pregnancy relate to the postpartum metabolic defects linking GDM with type 2 diabetes.Methods Metabolic characterisation, including oral glucose tolerance testing, was undertaken in 487 women during pregnancy and at 3 months postpartum. Based on the antepartum OGTT, there were 137 women with GDM, 91 with gestational impaired glucose tolerance and 259 with normal glucose tolerance. Results Adiponectin levels were lowest (p<0.0001) and CRP levels highest (p=0.0008) in women with GDM. Leptin did not differ between the glucose tolerance groups (p = 0.4483). Adiponectin (r = 0.41, p < 0.0001), leptin (r= −0.36, p <0.0001) and CRP (r = −0.30, p < 0.0001) during pregnancy were all associated with postpartum insulin sensitivity (determined using the insulin sensitivity index of Matsuda and DeFronzo [IS OGTT ]). Intriguingly, adiponectin levels were also related to postpartum beta cell function (insulinogenic index/HOMA of insulin resistance; r=0.16, p=0.0009). Indeed, on multiple linear regression analyses, adiponectin levels during pregnancy independently predicted both postpartum insulin sensitivity (t=3.97, p<0.0001) and beta cell function (t=2.37, p=0.0181), even after adjustment for GDM. Furthermore, adiponectin emerged as a significant negative independent determinant of postpartum fasting glucose (t=−3.01, p=0.0027). Conclusions/interpretation Hypoadiponectinaemia during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia, and hence may be relevant to the pathophysiology relating GDM with type 2 diabetes.

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“…A previous study reported progressive decline in maternal adiponectin secretion during the course of pregnancy which was associated with a 60 % reduction in adiponectin mRNA in white adipose tissue [38]. Reduced adiponectin levels in second and third trimesters compared to first trimester in healthy pregnant subjects was reported by many authors [38,39], although others reported unchanged values [22,29]. In the present study, unchanged maternal circulating adiponectin in normal pregnancy between 2nd and 3rd trimesters may represent an independent protective mechanism against the gradual increase in insulin resistance.…”

Section: Discussionmentioning

confidence: 94%

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

Cited by 240 publications

References 51 publications

Accretion of visceral fat and hepatic insulin resistance in pregnant rats

Accretion of visceral fat and hepatic insulin resistance in pregnant rats

Low adiponectin concentration during pregnancy predicts postpartum insulin resistance, beta cell dysfunction and fasting glycaemia

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

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