dc.date.accessioned | 2023-02-03T17:29:02Z | |
dc.date.available | 2023-02-03T17:29:02Z | |
dc.date.created | 2023-01-27T13:33:06Z | |
dc.date.issued | 2022 | |
dc.identifier.citation | Sommer, Christine Vangberg, Kjersti G. Moen, Gunn-Helen Øiseth Evans, David M. Lee-Ødegård, Sindre Høgestøl, Ingvild Kristine Sletner, Line Jenum, Anne Karen Drevon, Christian A. Gulseth, Hanne Løvdal Birkeland, Kåre Inge . Insulin and Body Mass Index Decrease Serum Soluble Leptin Receptor Levels in Humans. Journal of Clinical Endocrinology and Metabolism (JCEM). 2022 | |
dc.identifier.uri | http://hdl.handle.net/10852/99613 | |
dc.description.abstract | Abstract
Context
Serum soluble leptin receptor (sOb-R) may protect against future type 2 diabetes or serve as a marker for protective features, but how sOb-R is regulated is largely unknown.
Objective
This work aimed to test how serum sOb-R is influenced by glucose, insulin, body fat, body mass index (BMI), food intake, and physical activity.
Methods
We performed an epidemiological triangulation combining cross-sectional, interventional, and Mendelian randomization study designs. In 5 independent clinical studies (n = 24-823), sOb-R was quantified in serum or plasma by commercial enzyme-linked immunosorbent assay kits using monoclonal antibodies. We performed mixed-model regression and 2-sample Mendelian randomization.
Results
In pooled, cross-sectional data, leveling by study, sOb-R was associated inversely with BMI (β [95% CI] −0.19 [−0.21 to −0.17]), body fat (−0.12 [−0.14 to −0.10), and fasting C-peptide (−2.04 [−2.46 to −1.62]). sOb-R decreased in response to acute hyperinsulinemia during euglycemic glucose clamp in 2 independent clinical studies (−0.5 [−0.7 to −0.4] and −0.5 [−0.6 to −0.3]), and immediately increased in response to intensive exercise (0.18 [0.04 to 0.31]) and food intake (0.20 [0.06 to 0.34]). In 2-sample Mendelian randomization, higher fasting insulin and higher BMI were causally linked to lower sOb-R levels (inverse variance weighted, −1.72 [−2.86 to −0.58], and −0.20 [−0.36 to −0.04], respectively). The relationship between hyperglycemia and sOb-R was inconsistent in cross-sectional studies and nonsignificant in intervention studies, and 2-sample Mendelian randomization suggested no causal effect of fasting glucose on sOb-R.
Conclusion
BMI and insulin both causally decreased serum sOb-R levels. Conversely, intensive exercise and food intake acutely increased sOb-R. Our results suggest that sOb-R is involved in short-term regulation of leptin signaling, either directly or indirectly, and that hyperinsulinemia may reduce leptin signaling. | |
dc.language | EN | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 International | |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/4.0/ | |
dc.title | Insulin and Body Mass Index Decrease Serum Soluble Leptin Receptor Levels in Humans | |
dc.title.alternative | ENEngelskEnglishInsulin and Body Mass Index Decrease Serum Soluble Leptin Receptor Levels in Humans | |
dc.type | Journal article | |
dc.creator.author | Sommer, Christine | |
dc.creator.author | Vangberg, Kjersti G. | |
dc.creator.author | Moen, Gunn-Helen Øiseth | |
dc.creator.author | Evans, David M. | |
dc.creator.author | Lee-Ødegård, Sindre | |
dc.creator.author | Høgestøl, Ingvild Kristine | |
dc.creator.author | Sletner, Line | |
dc.creator.author | Jenum, Anne Karen | |
dc.creator.author | Drevon, Christian A. | |
dc.creator.author | Gulseth, Hanne Løvdal | |
dc.creator.author | Birkeland, Kåre Inge | |
cristin.unitcode | 185,51,13,0 | |
cristin.unitname | Avdeling for ernæringsvitenskap | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 2 | |
dc.identifier.cristin | 2116589 | |
dc.identifier.bibliographiccitation | info:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Journal of Clinical Endocrinology and Metabolism (JCEM)&rft.volume=&rft.spage=&rft.date=2022 | |
dc.identifier.jtitle | Journal of Clinical Endocrinology and Metabolism (JCEM) | |
dc.identifier.pagecount | 10 | |
dc.identifier.doi | https://doi.org/10.1210/clinem/dgac699 | |
dc.type.document | Tidsskriftartikkel | |
dc.type.peerreviewed | Peer reviewed | |
dc.source.issn | 0021-972X | |
dc.type.version | PublishedVersion | |
cristin.articleid | dgac699 | |