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Article: Obesity-resistance of UCP1-deficient mice associates with sustained FGF21 sensitivity in inguinal adipose tissue.

Klein Hazebroek, Marlou / Keipert, Susanne

2022 Volume 13, Page(s) 909621

Abstract: Metabolic diseases represent the major health burden of our modern society. With the need of novel therapeutic approaches, fibroblast growth factor 21 (FGF21) is a promising target, based on metabolic improvements upon FGF21 administration in mice and ... ...

Abstract	Metabolic diseases represent the major health burden of our modern society. With the need of novel therapeutic approaches, fibroblast growth factor 21 (FGF21) is a promising target, based on metabolic improvements upon FGF21 administration in mice and humans. Endogenous FGF21 serum levels, however, are increased during obesity-related diseases, suggesting the development of FGF21 resistance during obesity and thereby lowering FGF21 efficacy. In uncoupling protein 1 knockout (UCP1 KO) mice, however, elevated endogenous FGF21 levels mediate resistance against diet-induced obesity. Here, we show that after long-term high fat diet feeding (HFD), circulating FGF21 levels become similarly high in obese wildtype and obesity-resistant UCP1 KO mice, suggesting improved FGF21 sensitivity in UCP1 KO mice. To test this hypothesis, we injected FGF21 after long-term HFD and assessed the metabolic and molecular effects. The UCP1 KO mice lost weight directly upon FGF21 administration, whereas body weights of WT mice resisted weight loss in the initial phase of the treatment. The FGF21 treatment induced expression of liver
MeSH term(s)	Adipose Tissue ; Animals ; Diet, High-Fat ; Fibroblast Growth Factors ; Humans ; Mice ; Mice, Knockout ; Obesity ; Uncoupling Protein 1
Chemical Substances	UCP1 protein, human ; Ucp1 protein, mouse ; Uncoupling Protein 1 ; fibroblast growth factor 21 ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2022-08-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2022.909621
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Protection from alcohol intoxication: Must be FGF21 to enter.

Jastroch, Martin / Keipert, Susanne / Tschöp, Matthias H

Cell metabolism

2023 Volume 35, Issue 3, Page(s) 377–379

Abstract: Fibroblast growth factor 21 (FGF21) is generally known as a stress-induced metabolic regulator with enormous therapeutic potential to treat metabolic diseases, but a more specific role of FGF21 concerns physiological handling of alcohol in mammals. In ... ...

Abstract	Fibroblast growth factor 21 (FGF21) is generally known as a stress-induced metabolic regulator with enormous therapeutic potential to treat metabolic diseases, but a more specific role of FGF21 concerns physiological handling of alcohol in mammals. In this issue of Cell Metabolism, Choi et al. demonstrate that FGF21 mediates the recovery from alcohol intoxication by directly activating noradrenergic neurons in mice, thus advancing our knowledge on FGF21 biology and further diversifying its therapeutic potential.
MeSH term(s)	Mice ; Animals ; Alcoholic Intoxication ; Fibroblast Growth Factors/metabolism ; Ethanol ; Metabolic Diseases ; Mammals/metabolism
Chemical Substances	fibroblast growth factor 21 ; Fibroblast Growth Factors (62031-54-3) ; Ethanol (3K9958V90M)
Language	English
Publishing date	2023-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2023.02.010
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Article ; Online: Stress-induced FGF21 and GDF15 in obesity and obesity resistance.

Keipert, Susanne / Ost, Mario

Trends in endocrinology and metabolism: TEM

2021 Volume 32, Issue 11, Page(s) 904–915

Abstract: Fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15) are established as stress-responsive cytokines that can modulate energy balance by increasing energy expenditure or suppressing food intake, respectively. Despite their ... ...

Abstract	Fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15) are established as stress-responsive cytokines that can modulate energy balance by increasing energy expenditure or suppressing food intake, respectively. Despite their pharmacologically induced beneficial effects on obesity and comorbidities, circulating levels of both cytokines are elevated during obesity and related metabolic complications. On the other hand, endocrine crosstalk via FGF21 and GDF15 was also reported to play a crucial role in genetically modified mouse models of mitochondrial perturbations leading to diet-induced obesity (DIO) resistance. This review aims to dissect the complexities of endogenous FGF21 and GDF15 action in obesity versus DIO resistance for the regulation of energy balance in metabolic health and disease.
MeSH term(s)	Animals ; Energy Metabolism/physiology ; Fibroblast Growth Factors/genetics ; Fibroblast Growth Factors/metabolism ; Growth Differentiation Factor 15/genetics ; Growth Differentiation Factor 15/metabolism ; Humans ; Mice ; Obesity/metabolism ; Stress, Physiological
Chemical Substances	GDF15 protein, human ; Gdf15 protein, mouse ; Growth Differentiation Factor 15 ; fibroblast growth factor 21 ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2021-09-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2021.08.008
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Zs.A 2999: Show issues

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Article: Adapting to the Cold: A Role for Endogenous Fibroblast Growth Factor 21 in Thermoregulation?

Klein Hazebroek, Marlou / Keipert, Susanne

Frontiers in endocrinology

2020 Volume 11, Page(s) 389

Abstract: Fibroblast growth factor 21 (FGF21) is in biomedical focus as a treatment option for metabolic diseases, given that administration improves metabolism in mice and humans. The metabolic effects of exogenous FGF21 administration are well-characterized, but ...

Abstract	Fibroblast growth factor 21 (FGF21) is in biomedical focus as a treatment option for metabolic diseases, given that administration improves metabolism in mice and humans. The metabolic effects of exogenous FGF21 administration are well-characterized, but the physiological role of endogenous FGF21 has not been fully understood yet. Despite cold-induced FGF21 expression and increased circulating levels in some studies, which co-occur with brown fat thermogenesis, recent studies in cold-acclimated mice demonstrate the dispensability of FGF21 for maintenance of body temperature, thereby questioning FGF21's role for thermogenesis. Here we discuss the evidence either supporting or opposing the role of endogenous FGF21 for thermogenesis based on the current literature. FGF21, secreted by brown fat or liver, is likely not required for energy homeostasis in the cold, but the nutritional conditions could modulate the interaction between FGF21, energy metabolism, and thermoregulation.
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Animals ; Body Temperature Regulation ; Cold Temperature ; Endocrine System/metabolism ; Energy Metabolism ; Fibroblast Growth Factors/metabolism ; Humans ; Liver/metabolism ; Paracrine Communication
Chemical Substances	fibroblast growth factor 21 ; Fibroblast Growth Factors (62031-54-3)
Language	English
Publishing date	2020-07-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2020.00389
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Article ; Online: Gut Microbes Controlling Blood Sugar: No Fire Required!

Jastroch, Martin / Ussar, Siegfried / Keipert, Susanne

Cell metabolism

2020 Volume 31, Issue 3, Page(s) 443–444

Abstract: The gut microbiota plays an important role for the absorption of nutrients and the maintenance of metabolism, potentially impacting the development of human metabolic disorders such as obesity and type 2 diabetes. In this issue of Cell Metabolism, Krisko ...

Abstract	The gut microbiota plays an important role for the absorption of nutrients and the maintenance of metabolism, potentially impacting the development of human metabolic disorders such as obesity and type 2 diabetes. In this issue of Cell Metabolism, Krisko et al. (2020) demonstrate that the gut microbiota regulates glucose homeostasis solely via hepatic gluconeogenesis and not via thermogenic adipose tissue as suggested previously.
MeSH term(s)	Animals ; Blood Glucose ; Diabetes Mellitus, Type 2 ; Gastrointestinal Microbiome ; Homeostasis ; Humans ; Mice ; Microbiota ; Thermogenesis
Chemical Substances	Blood Glucose
Language	English
Publishing date	2020-03-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2020.02.007
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Article ; Online: Hyperphagia of female UCP1-deficient mice blunts anti-obesity effects of FGF21.

Klein Hazebroek, Marlou / Laterveer, Rutger / Kutschke, Maria / Ramšak Marčeta, Vida / Barthem, Clarissa S / Keipert, Susanne

Scientific reports

2023 Volume 13, Issue 1, Page(s) 10288

Abstract: Increasing energy expenditure through uncoupling protein 1 (UCP1) activity in thermogenic adipose tissue is widely investigated to correct diet-induced obesity (DIO). Paradoxically, UCP1-deficient male mice are resistant to DIO at room temperature. ... ...

Abstract	Increasing energy expenditure through uncoupling protein 1 (UCP1) activity in thermogenic adipose tissue is widely investigated to correct diet-induced obesity (DIO). Paradoxically, UCP1-deficient male mice are resistant to DIO at room temperature. Recently, we uncovered a key role for fibroblast growth factor 21 (FGF21), a promising drug target for treatment of metabolic disease, in this phenomenon. As the metabolic action of FGF21 is so far understudied in females, we aim to investigate potential sexual dimorphisms. Here, we confirm that male UCP1 KO mice display resistance to DIO in mild cold, without significant changes in metabolic parameters. Surprisingly, females gained the same amount of body fat as WT controls. Molecular regulation was similar between UCP1 KO males and females, with an upregulation of serum FGF21, coinciding with beiging of inguinal white adipose tissue and induced lipid metabolism. While energy expenditure did not display significant differences, UCP1 KO females significantly increased their food intake. Altogether, our results indicate that hyperphagia is likely counteracting the beneficial effects of FGF21 in female mice. This underlines the importance of sex-specific studies in (pre)clinical research for personalized drug development.
MeSH term(s)	Animals ; Female ; Male ; Mice ; Hyperphagia/drug therapy ; Mice, Knockout ; Obesity/drug therapy ; Obesity/etiology ; Obesity/metabolism ; Uncoupling Protein 1/genetics ; Uncoupling Protein 1/metabolism
Chemical Substances	fibroblast growth factor 21 ; Uncoupling Protein 1 ; Ucp1 protein, mouse
Language	English
Publishing date	2023-06-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-37264-0
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Article ; Online: Brown adipose tissue-derived metabolites and their role in regulating metabolism.

Ziqubu, Khanyisani / Dludla, Phiwayinkosi V / Mabhida, Sihle E / Jack, Babalwa U / Keipert, Susanne / Jastroch, Martin / Mazibuko-Mbeje, Sithandiwe E

Metabolism: clinical and experimental

2023 Volume 150, Page(s) 155709

Abstract: The discovery and rejuvenation of metabolically active brown adipose tissue (BAT) in adult humans have offered a new approach to treat obesity and metabolic diseases. Beyond its accomplished role in adaptive thermogenesis, BAT secretes signaling ... ...

Abstract	The discovery and rejuvenation of metabolically active brown adipose tissue (BAT) in adult humans have offered a new approach to treat obesity and metabolic diseases. Beyond its accomplished role in adaptive thermogenesis, BAT secretes signaling molecules known as "batokines", which are instrumental in regulating whole-body metabolism via autocrine, paracrine, and endocrine action. In addition to the intrinsic BAT metabolite-oxidizing activity, the endocrine functions of these molecules may help to explain the association between BAT activity and a healthy systemic metabolic profile. Herein, we review the evidence that underscores the significance of BAT-derived metabolites, especially highlighting their role in controlling physiological and metabolic processes involving thermogenesis, substrate metabolism, and other essential biological processes. The conversation extends to their capacity to enhance energy expenditure and mitigate features of obesity and its related metabolic complications. Thus, metabolites derived from BAT may provide new avenues for the discovery of metabolic health-promoting drugs with far-reaching impacts. This review aims to dissect the complexities of the secretory role of BAT in modulating local and systemic metabolism in metabolic health and disease.
MeSH term(s)	Humans ; Adipose Tissue, Brown/metabolism ; Obesity/metabolism ; Energy Metabolism/physiology ; Metabolic Diseases/metabolism ; Signal Transduction ; Thermogenesis/physiology
Language	English
Publishing date	2023-10-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80230-x
ISSN	1532-8600 ; 0026-0495
ISSN (online)	1532-8600
ISSN	0026-0495
DOI	10.1016/j.metabol.2023.155709
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Book ; Thesis: The effects of mitochondrial uncoupling in skeletal muscle on lifespan, substrate and energy metabolism in mice

Keipert, Susanne

2011

Author's details	von Susanne Keipert
Language	English
Size	75 Bl., Ill., graph. Darst.
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Potsdam, 2011
Database	Special collection on veterinary medicine and general parasitology

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Article ; Online: Insights into brown adipose tissue evolution and function from non-model organisms.

Jastroch, Martin / Oelkrug, Rebecca / Keipert, Susanne

The Journal of experimental biology

2018 Volume 221, Issue Pt Suppl 1

Abstract: Brown adipose tissue (BAT) enables adaptive thermoregulation through heat production that is catalyzed by mitochondrial uncoupling protein 1 (UCP1). BAT is frequently studied in rodent model organisms, and recently in adult humans to treat metabolic ... ...

Abstract	Brown adipose tissue (BAT) enables adaptive thermoregulation through heat production that is catalyzed by mitochondrial uncoupling protein 1 (UCP1). BAT is frequently studied in rodent model organisms, and recently in adult humans to treat metabolic diseases. However, complementary studies of many non-model species, which have diversified to many more ecological niches, may significantly broaden our understanding of BAT regulation and its physiological roles. This Review highlights the research on non-model organisms, which was instrumental to the discovery of BAT function, and the unique evolutionary history of BAT/UCP1 in mammalian thermogenesis. The comparative biology of BAT provides a powerful integrative approach that could identify conserved and specialized functional changes in BAT and UCP1 by considering species diversity, ecology and evolution, and by fusing multiple scientific disciplines such as physiology and biochemistry. Thus, resolving the complete picture of BAT biology may fail if comparative studies of non-model organisms are neglected.
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Animals ; Biological Evolution ; Mammals/physiology ; Thermogenesis/physiology ; Uncoupling Protein 1/genetics ; Uncoupling Protein 1/metabolism
Chemical Substances	Uncoupling Protein 1
Language	English
Publishing date	2018-03-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218085-6
ISSN	1477-9145 ; 0022-0949
ISSN (online)	1477-9145
ISSN	0022-0949
DOI	10.1242/jeb.169425
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Zs.A 2629: Show issues

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Article ; Online: Decreased methylglyoxal-mediated protein glycation in the healthy aging mouse model of ectopic expression of UCP1 in skeletal muscle.

Masania, Jinit / Wijten, Patrick / Keipert, Susanne / Ost, Mario / Klaus, Susanne / Rabbani, Naila / Thornalley, Paul J

Redox biology

2022 Volume 59, Page(s) 102574

Abstract: Mice with ectopic expression of uncoupling protein-1 (UCP1) in skeletal muscle exhibit a healthy aging phenotype with increased longevity and resistance to impaired metabolic health. This may be achieved by decreasing protein glycation by the reactive ... ...

Abstract	Mice with ectopic expression of uncoupling protein-1 (UCP1) in skeletal muscle exhibit a healthy aging phenotype with increased longevity and resistance to impaired metabolic health. This may be achieved by decreasing protein glycation by the reactive metabolite, methylglyoxal (MG). We investigated protein glycation and oxidative damage in skeletal muscle of mice with UCP1 expression under control of the human skeletal actin promoter (HSA-mUCP1) at age 12 weeks (young) and 70 weeks (aged). We found both young and aged HSA-mUCP1 mice had decreased advanced glycation endproducts (AGEs) formed from MG, lysine-derived N
MeSH term(s)	Humans ; Mice ; Animals ; Aged ; Infant ; Glycation End Products, Advanced/metabolism ; Lysine/metabolism ; Pyruvaldehyde/metabolism ; Maillard Reaction ; Healthy Aging ; Uncoupling Protein 1/metabolism ; Ectopic Gene Expression ; Proteins/metabolism ; Muscle, Skeletal/metabolism ; Tumor Suppressor Proteins/metabolism ; Ubiquitin-Protein Ligases/metabolism
Chemical Substances	Glycation End Products, Advanced ; Lysine (K3Z4F929H6) ; Pyruvaldehyde (722KLD7415) ; Uncoupling Protein 1 ; Proteins ; UCP1 protein, human ; HUWE1 protein, human (EC 2.3.2.26) ; Tumor Suppressor Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Ucp1 protein, mouse
Language	English
Publishing date	2022-12-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2022.102574
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