Central and peripheral leptin and agouti‐related protein during and after pregnancy in relation to weight change

Andersson‐Hall, Ulrika; Svedin, Pernilla; Andréasson, Ulf; Gren, Magnus; Ingemansson, Ameli; Zetterberg, Henrik; Blennow, Kaj; Pelanis, Aurimantas; Mallard, Carina; Holmäng, Agneta

doi:10.1111/cen.13520

Cited by 9 publications

(5 citation statements)

References 31 publications

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“…16 A recent longitudinal study reported an increase in CSF:peripheral leptin ratio after delivery, and indicated that peripheral AgRP levels in late pregnancy might predict longer-term (5 year) weight changes. 17 The finding that circulating leptin at delivery was associated with maternal weight and GWG is consistent with other studies which have reported cross-sectional associations between maternal leptin and GWG in different populations or time points, including at 10-20, 30 and 36 weeks, in adults and adolescents, across a range of BMI categories. [18][19][20][21] Some of these studies also reported significant correlations between maternal circulating leptin in late pregnancy and maternal weight or fat mass prior to and in late pregnancy, consistent with our findings.…”

Section: Discussionsupporting

confidence: 90%

<p>Exploring the Relationship Between Maternal Circulating Hormones and Gestational Weight Gain in Women Without Obesity: A Cross-Sectional Study</p>

Lappas

Lim

Price

et al. 2020

IJWH

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Background: Central homeostatic regulation of fat stores is attenuated during pregnancy, to allow for adequate fat deposition to support fetal development and lactation. What factors particular to pregnancy facilitate fat accumulation, and why gestational weight gain (GWG) is so variable, are not clear. The aim of this cross-sectional study was to examine the associations between GWG and circulating hormones with known effects on appetite and growth. Methods: Women without obesity (body mass index, BMI <30 kg/m 2), with a healthy singleton pregnancy, were recruited at the time of delivery by elective Caesarean section at a tertiary obstetric hospital. Women with preterm (<37 weeks) delivery and smokers were excluded. Maternal blood was collected at the time of delivery for measurement of fasting oestradiol, progesterone, prolactin, insulin, leptin, insulin-like growth factor 1 and insulinlike growth factor binding protein 3. Comparisons were made between women who gained weight within the range recommended by Institute of Medicine guidelines for normal weight women (11.5-16 kg; n=34) and those who gained excessive weight (>16 kg; n=35) during pregnancy. Analysis of covariance was carried out using multiple linear regression to test the effect of GWG group on biochemical parameters, accounting for pre-pregnancy BMI. Results: The 69 participants had a mean age of 34.6 ± 4.3 years, and pre-pregnancy BMI of (23.3 ± 1.8 kg/m 2), with no significant differences between groups in pre-pregnancy weight, BMI, age, birthweight or parity. Mean GWG was 14.0 ± 1.3 kg in the "recommended" group and 19.6 ± 3.2 kg in the "excessive" group. Leptin was significantly higher (43.4 ± 21.6 vs 33.4 ± 15.0 ng/mL, p=0.03) and prolactin tended to be lower (159.5 ± 66.1 vs 194.0 ± 85.6 ng/mL, p=0.07) at delivery in women with excessive (vs recommended) GWG. No other circulating factors were found to differ between groups. The between-group difference in leptin remained after adjustment for pre-pregnancy BMI in multiple linear regression and quantile regression analyses. Conclusion: In women without obesity, leptin remains a marker of adiposity during pregnancy. GWG was not associated with other circulating hormones with effects on appetite and growth.

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Section: Discussionsupporting

confidence: 90%

<p>Exploring the Relationship Between Maternal Circulating Hormones and Gestational Weight Gain in Women Without Obesity: A Cross-Sectional Study</p>

Lappas

Lim

Price

et al. 2020

IJWH

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“…Women were recruited at admission for elective cesarean section as previously described [ 19 ], and followed up 5 years after pregnancy [ 29 ]. All women with serum and/or CSF samples available from the previous study were included in the present study.…”

Section: Methodsmentioning

confidence: 99%

Growth differentiation factor 15 increases in both cerebrospinal fluid and serum during pregnancy

et al. 2021

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Aim Growth differentiation factor 15 (GDF15) increases in serum during pregnancy to levels not seen in any other physiological state and is suggested to be involved in pregnancy-induced nausea, weight regulation and glucose metabolism. The main action of GDF15 is regulated through a receptor of the brainstem, i.e., through exposure of GDF15 in both blood and cerebrospinal fluid (CSF). The aim of the current study was to measure GDF15 in both CSF and serum during pregnancy, and to compare it longitudinally to non-pregnant levels. Methods Women were sampled at elective caesarean section (n = 45, BMI = 28.1±5.0) and were followed up 5 years after pregnancy (n = 25). GDF15, insulin and leptin were measured in CSF and serum. Additional measurements included plasma glucose, and serum adiponectin and Hs-CRP. Results GDF15 levels were higher during pregnancy compared with follow-up in both CSF (385±128 vs. 115±32 ng/l, P<0.001) and serum (73789±29198 vs. 404±102 ng/l, P<0.001). CSF levels correlated with serum levels during pregnancy (P<0.001), but not in the non-pregnant state (P = 0.98). Both CSF and serum GDF15 were highest in women carrying a female fetus (P<0.001). Serum GDF15 correlated with the homeostatic model assessment for beta-cell function and placental weight, and CSF GDF15 correlated inversely with CSF insulin levels. Conclusion This, the first study to measure CSF GDF15 during pregnancy, demonstrated increased GDF15 levels in both serum and CSF during pregnancy. The results suggest that effects of GDF15 during pregnancy can be mediated by increases in both CSF and serum levels.

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“…Membrane‐bound short iso‐forms of the OB‐R are believed to mediate leptin transport over the BBB, and sOB‐R regulates transport by preventing clearance of leptin from the circulation 12,30 . There are also indications of altered BBB leptin transport in pregnancy, as the leptin ratio between cerebrospinal fluid and serum is reduced compared with the non‐pregnant state 32–34 . Gustafson et al 35 further demonstrated in an animal study that leptin transport from the peripheral circulation to hypothalamus was completely suppressed in late pregnancy.…”

Section: Discussionmentioning

confidence: 99%

“…12,30 There are also indications of altered BBB leptin transport in pregnancy, as the leptin ratio between cerebrospinal fluid and serum is reduced compared with the non-pregnant state. [32][33][34] Gustafson et al 35 further demonstrated in an animal study that leptin transport from the peripheral circulation to hypothalamus was completely suppressed in late pregnancy. Impaired BBB leptin transport is thereby relevant to consider as a mechanism to target in prevention of eGWG.…”

Section: Excessive and Leptin Resistancementioning

confidence: 98%

Gestational weight gain, appetite regulating hormones, and metformin treatment in polycystic ovary syndrome: A longitudinal, placebo‐controlled study

Molin

Løvvik

Dehlin

et al. 2021

BJOG

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Central and peripheral leptin and agouti‐related protein during and after pregnancy in relation to weight change

Abstract: S-AgRP concentration in late pregnancy may be one factor predicting weight change after pregnancy, and circulating AgRP may be physiologically important in the long-term regulation of body weight.

Cited by 9 publications

References 31 publications

<p>Exploring the Relationship Between Maternal Circulating Hormones and Gestational Weight Gain in Women Without Obesity: A Cross-Sectional Study</p>

<p>Exploring the Relationship Between Maternal Circulating Hormones and Gestational Weight Gain in Women Without Obesity: A Cross-Sectional Study</p>

Growth differentiation factor 15 increases in both cerebrospinal fluid and serum during pregnancy

Gestational weight gain, appetite regulating hormones, and metformin treatment in polycystic ovary syndrome: A longitudinal, placebo‐controlled study

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