Mette Bjerre

Increased leptin, decreased adiponectin and FGF21 concentrations in adolescent offspring of women with gestational diabetes

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

DOI

  • Freja Bach Kampmann, F Kampmann, Department of Endocrinology, Rigshospitalet, Kobenhavn, Denmark.
  • ,
  • Anne Cathrine Baun Thuesen, A Thuesen, Clinical,metabolic, physiology, Steno Diabetes Center Copenhagen, Gentofte, Denmark.
  • ,
  • Line Hjort, L Hjort, Department of Obstetrics, Rigshospitalet, Kobenhavn, Denmark.
  • ,
  • Anne Ahrendt Bjerregaard, A Bjerregaard, Centre for Fetal Programming, Department of Epidemiology Research, Statens Serum Institut, Copenhagen, Denmark.
  • ,
  • Jorge Chavarro, J Chavarro, Department of Nutrition and Epidemiology, Harvard University Boston Area Research Initiative, Boston, United States.
  • ,
  • Jan Frystyk
  • Mette Bjerre
  • Inge Tetens, I Tetens, Vitality - Centre for Good Older Lives, Department of Nutrion, Sports and Exercise, University of Copenhagen, Kobenhavns, Denmark.
  • ,
  • Sjurdur Olsen, S Olsen, Department of Epidemiology Research, Centre for Fetal Programming, Statens Serum Institut, Copenhagen, Denmark.
  • ,
  • Allan Vaag, A Vaag, Translational Research and Early Clinical Development, AstraZeneca Pharmaceuticals, Gothenburg, Sweden.
  • ,
  • Peter Damm, P Damm, Center for Pregnant Women with Diabetes, Department of Obstetrics, Rigshospitalet, Kobenhavn, Denmark.
  • ,
  • Louise Groth Grunnet, L Grunnet, Department of Diabetes and Metabolism, Rigshospitalet, Copenhagen, Denmark.

OBJECTIVE: Fetal exposure to gestational diabetes mellitus (GDM) increases the risk of metabolic diseases in the offspring. Leptin, adiponectin, and fibroblast growth factor 21 (FGF21) may play potential roles in the underlying disease mechanisms. We investigated the impact of fetal exposure to GDM on leptin, adiponectin, and FGF21 concentrations and their associations with measures of adiposity and metabolic traits during childhood/adolescence.

DESIGN AND METHODS: The follow-up study included 504 GDM and 540 control offspring aged 9-16 from the Danish National Birth Cohort. Anthropometric measurements, fasting blood samples, puberty status and fat percentages by Dual-energy x-ray absorptiometry were examined. Serum concentrations of leptin, adiponectin, and FGF21 were measured by validated immune assays.

RESULTS: GDM offspring had 38% (95% CI: 22-55%) higher leptin, 0.6mg/L (95% CI -1.2, -0.04mg/L) lower adiponectin, and 32% (95% CI: -47%, -12%) lower FGF21 concentrations than control offspring (p<0.05). After adjustment for confounders including maternal pre-pregnancy BMI, GDM offspring had borderline higher leptin (p=0.06) and significantly lower FGF21 concentrations (p=0.006). When accounting for offspring BMI z-score, GDM exposure had no significant independent effect on leptin or adiponectin concentrations whereas FGF21 was still significant. In univariate analyses, leptin and adiponectin were associated with fasting insulin, HOMA-IR, and adiposity, and FGF21 with total fat percentage.

CONCLUSIONS: GDM offspring had higher leptin, lower adiponectin and FGF21 concentrations than control offspring. Elevated leptin and decreased adiponectin concentrations associated with adverse metabolic traits and were most likely driven by higher obesity prevalence among GDM offspring. The functional implications of decreased FGF21 concentrations among GDM offspring need to be further explored.

OriginalsprogEngelsk
TidsskriftEuropean Journal of Endocrinology
Vol/bind181
Nummer6
Sider (fra-til)691-700
Antal sider10
ISSN0804-4643
DOI
StatusUdgivet - dec. 2019

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