Evidence map›Paper›PMID 40169533›Full record

ArticleBone research2025

KIAA1199 (CEMIP) regulates adipogenesis and whole-body energy metabolism.

Li Chen, Kaikai Shi, Nicholas Ditzel, Weimin Qiu, Michaela Tencerova, Louise Himmelstrup Dreyer Nielsen, Florence Figeac, Alexander Rauch, Yuhang Liu, Jiuyuan Tao and 8 more

Abstract read
In one paragraph

Article in Bone research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Li ChenGuangxi Key Laboratory of Tumor Immunology and Microenvironment Regulation, Guilin Medical University, Guilin, Guangxi, 541199, China. chenli@glmc.edu.cn.ORCID http://orcid.org/0000-0001-5561-7612
Kaikai ShiDepartment of Endocrinology and Metabolism, Endocrine Research Laboratory (KMEB), Odense University Hospital & University of Southern Denmark, Odense, Dk-5230, Denmark.
Nicholas DitzelDepartment of Endocrinology and Metabolism, Endocrine Research Laboratory (KMEB), Odense University Hospital & University of Southern Denmark, Odense, Dk-5230, Denmark.
Weimin QiuDepartment of Endocrinology and Metabolism, Endocrine Research Laboratory (KMEB), Odense University Hospital & University of Southern Denmark, Odense, Dk-5230, Denmark.
Michaela TencerovaDepartment of Endocrinology and Metabolism, Endocrine Research Laboratory (KMEB), Odense University Hospital & University of Southern Denmark, Odense, Dk-5230, Denmark.ORCID http://orcid.org/0000-0001-8670-425X
Louise Himmelstrup Dreyer NielsenDepartment of Endocrinology and Metabolism, Endocrine Research Laboratory (KMEB), Odense University Hospital & University of Southern Denmark, Odense, Dk-5230, Denmark.
Florence FigeacDepartment of Endocrinology and Metabolism, Endocrine Research Laboratory (KMEB), Odense University Hospital & University of Southern Denmark, Odense, Dk-5230, Denmark.ORCID http://orcid.org/0000-0001-7244-9438
Alexander RauchDepartment of Endocrinology and Metabolism, Endocrine Research Laboratory (KMEB), Odense University Hospital & University of Southern Denmark, Odense, Dk-5230, Denmark.ORCID http://orcid.org/0000-0002-9429-7356
Yuhang LiuGuangxi Key Laboratory of Tumor Immunology and Microenvironment Regulation, Guilin Medical University, Guilin, Guangxi, 541199, China.
Jiuyuan TaoGuangxi Key Laboratory of Tumor Immunology and Microenvironment Regulation, Guilin Medical University, Guilin, Guangxi, 541199, China.
Veronika SramkovaDepartment of Pathophysiology, Centre for Research on Diabetes, Metabolism and Nutrition, Third Faculty of Medicine, Charles University, Prague, Czech Republic.
Lenka RossmeislovaDepartment of Pathophysiology, Centre for Research on Diabetes, Metabolism and Nutrition, Third Faculty of Medicine, Charles University, Prague, Czech Republic.
Greet KerckhofsBiomechanics Lab, Institute of Mechanics, Materials, and Civil Engineering, KU Leuven, Leuven, Belgium.
Tatjana N Parac-VogtBiomechanics Lab, Institute of Mechanics, Materials, and Civil Engineering, KU Leuven, Leuven, Belgium.
Sébastien de BournonvilleBiomechanics Section, Department of Mechanical Engineering, KU Leuven, Leuven, Belgium.
Thomas Levin AndersenInstitute of Pathology, University of Southern Denmark, Odense, Denmark.ORCID http://orcid.org/0000-0002-6981-7276
Mikael RydénDepartment of Medicine (H7), Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
Moustapha KassemDepartment of Endocrinology and Metabolism, Endocrine Research Laboratory (KMEB), Odense University Hospital & University of Southern Denmark, Odense, Dk-5230, Denmark. mkassem@health.sdu.dk.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32060155National Natural Science Foundation of China (National Science Foundation of China) 82260284Novo Nordisk Fonden (Novo Nordisk Foundation) NNF15OC0016284Novo Nordisk Fonden (Novo Nordisk Foundation) NNF19OC0057449
6 · The paper itself

Abstract

An increasing number of studies have characterized the bone as an endocrine organ, and that bone secreted factors may not only regulate local bone remodeling, but also other tissues and whole-body metabolic functions. The precise nature of these regulatory factors and their roles at bridging the bone, bone marrow adipose tissue, extramedullary body fat and whole-body energy homeostasis are being explored. In this study, we report that KIAA1199, a secreted factor produced from bone and bone marrow, previously described as an inhibitor of bone formation, also plays a role at promoting adipogenesis. KIAA1199-deficient mice exhibit reduced bone marrow adipose tissue, subcutaneous and visceral fat tissue mass, blood cholesterol, triglycerides, free fatty acids and glycerol, as well as improved insulin sensitivity in skeletal muscle, liver and fat. Moreover, these mice are protected from the detrimental effects of high-fat diet feeding, with decreased obesity, lower blood glucose and glucose tolerance, as well as decreased adipose tissue inflammation, insulin resistance and hepatic steatosis. In human studies, plasma levels of KIAA1199 or its expression levels in adipose tissue are positively correlated with insulin resistance and blood levels of cholesterol, triglycerides, free fatty acids, glycerol, fasting glucose and HOMA-IR. Mechanistically, KIAA1199 mediates its effects on adipogenesis through modulating osteopontin-integrin and AKT / ERK signaling. These findings provide evidence for the role of bone secreted factors on coupling bone, fat and whole-body energy homeostasis.

Indexed as

AdipogenesisEnergy MetabolismProteinsAdipose TissueAnimalsDiet, High-FatHumansHyaluronoglucosaminidaseInsulin ResistanceMaleMiceMice, Inbred C57BLObesityCEMIP protein, humanHyaluronoglucosaminidaseProteins

Identifiers

PMID40169533
PMCPMC11961601

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.