Acute fat loss does not affect bone mass
|Author:||Lagerquist, Marie K.1; Gustafsson, Karin L.1; Henning, Petra1;|
1Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Su Sahlgrenska, Vita Stråket 11, 413 45, Gothenburg, Sweden
2Department of Anatomy and Cell Biology, Cancer and Translational Medicine Research Unit, University of Oulu, Oulu, Finland
3Unit of Metabolic Physiology, Department of Physiology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
|Online Access:||PDF Full Text (PDF, 1.1 MB)|
|Persistent link:|| http://urn.fi/urn:nbn:fi-fe2021090945664
|Publish Date:|| 2021-09-09
Obesity has previously been thought to protect bone since high body weight and body mass index are associated with high bone mass. However, some more recent studies suggest that increased adiposity negatively impacts bone mass. Here, we aimed to test whether acute loss of adipose tissue, via adipocyte apoptosis, alters bone mass in age-related obese mice. Adipocyte apoptosis was induced in obese male FAT-ATTAC mice through AP20187 dimerizer-mediated activation of caspase 8 selectively in adipocytes. In a short-term experiment, dimerizer was administered to 5.5 month-old mice that were terminated 2 weeks later. At termination, the total fat mass weighed 58% less in dimerizer-treated mice compared with vehicle-treated controls, but bone mass did not differ. To allow for the detection of long-term effects, we used 9-month-old mice that were terminated six weeks after dimerizer administration. In this experiment, the total fat mass weighed less (− 68%) in the dimerizer-treated mice than in the controls, yet neither bone mass nor biomechanical properties differed between groups. Our findings show that adipose tissue loss, despite the reduced mechanical loading, does not affect bone in age-related obese mice. Future studies are needed to test whether adipose tissue loss is beneficial during more severe obesity.
|Type of Publication:||
A1 Journal article – refereed
|Field of Science:||
Open access funding provided by University of Gothenburg. This work was supported by the Sahlgrenska University Hospital foundation, O.E. and Edla Johansson’s Scientific Foundation, Wilhelm and Martina Lundgrens’s Science Fund (grant number: 2016-1334), Längmanska Foundation (Grant Number BA17-0597), Sigurd and Elsa Golje’s Memory Foundation (Grant Number: LA2016-0470), and Lars Hierta’s Memory Foundation (Grant Number: FO2016-0036), Gustaf V’s 80-years fund (FAI-2016-0286), the Swedish Diabetes Foundation (DIA2019-419), Swedish research council (2017-01286, 2017-00792, 2020-01463, and 2013-7107), NovoNordisk Foundation (NNF17OC0026844 and NNF19OC0056601), and IngaBritt and Arne Lundgren Foundation.
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