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Adiponectin protects against development of metabolic disturbances in a PCOS mouse model

Artikel i vetenskaplig tidskrift
Författare Anna Benrick
Belén Chanclón
Peter Micallef
Yanling Wu
Laila Hadi
J. M. Shelton
Elisabet Stener-Victorin
Ingrid Wernstedt Asterholm
Publicerad i Proceedings of the National Academy of Sciences of the United States of America
Volym 114
Nummer/häfte 34
Sidor E7187-E7196
ISSN 0027-8424
Publiceringsår 2017
Publicerad vid Institutionen för neurovetenskap och fysiologi
Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Sidor E7187-E7196
Språk en
Länkar doi.org/10.1073/pnas.1708854114
Ämnesord polycystic ovary syndrome, insulin resistance, adipose tissue, polycystic-ovary-syndrome, impaired glucose-tolerance, genome-wide, association, omental fat expression, adipose-tissue, insulin-resistance, transcription factors, skeletal-muscle, gene-expression, nonobese women, Science & Technology - Other Topics
Ämneskategorier Klinisk medicin

Sammanfattning

Adiponectin, together with adipocyte size, is the strongest factor associated with insulin resistance in women with polycystic ovary syndrome (PCOS). This study investigates the causal relationship between adiponectin levels and metabolic and reproductive functions in PCOS. Prepubertal mice overexpressing adiponectin from adipose tissue (APNtg), adiponectin knockouts (APNko), and their wild-type (WT) littermate mice were continuously exposed to placebo or dihydrotestosterone (DHT) to induce PCOS-like traits. As expected, DHT exposure led to reproductive dysfunction, as judged by continuous anestrus, smaller ovaries with a decreased number of corpus luteum, and an increased number of cystic/atretic follicles. A two-way between-groups analysis showed that there was a significant main effect for DHT exposure, but not for genotype, indicating adiponectin does not influence follicle development. Adiponectin had, however, some protective effects on ovarian function. Similar to in many women with PCOS, DHT exposure led to reduced adiponectin levels, larger adipocyte size, and reduced insulin sensitivity in WTs. APNtg mice remained metabolically healthy despite DHT exposure, while APNko-DHT mice were even more insulin resistant than their DHT-exposed littermate WTs. DHT exposure also reduced the mRNA expression of genes involved in metabolic pathways in gonadal adipose tissue of WT and APNko, but this effect of DHT was not observed in APNtg mice. Moreover, APNtg-DHT mice displayed increased pancreatic mRNA levels of insulin receptors, Pdx1 and Igf1R, suggesting adiponectin stimulates beta cell viability/hyperplasia in the context of PCOS. In conclusion, adiponectin improves metabolic health but has only minor effects on reproductive functions in this PCOS-like mouse model.

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