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Article ; Online: The GDF15-GFRAL pathway is dispensable for the effects of metformin on energy balance.

Klein, Anders B / Nicolaisen, Trine S / Johann, Kornelia / Fritzen, Andreas M / Mathiesen, Cecilie V / Gil, Cláudia / Pilmark, Nanna S / Karstoft, Kristian / Blond, Martin B / Quist, Jonas S / Seeley, Randy J / Færch, Kristine / Lund, Jens / Kleinert, Maximilian / Clemmensen, Christoffer

Cell reports

2022 Volume 40, Issue 8, Page(s) 111258

Abstract: Metformin is a blood-glucose-lowering medication with physiological effects that extend beyond its anti-diabetic indication. Recently, it was reported that metformin lowers body weight via induction of growth differentiation factor 15 (GDF15), which ... ...

Abstract	Metformin is a blood-glucose-lowering medication with physiological effects that extend beyond its anti-diabetic indication. Recently, it was reported that metformin lowers body weight via induction of growth differentiation factor 15 (GDF15), which suppresses food intake by binding to the GDNF family receptor α-like (GFRAL) in the hindbrain. Here, we corroborate that metformin increases circulating GDF15 in mice and humans, but we fail to confirm previous reports that the GDF15-GFRAL pathway is necessary for the weight-lowering effects of metformin. Instead, our studies in wild-type, GDF15 knockout, and GFRAL knockout mice suggest that the GDF15-GFRAL pathway is dispensable for the effects of metformin on energy balance. The data presented here question whether metformin is a sufficiently strong stimulator of GDF15 to drive anorexia and weight loss and emphasize that additional work is needed to untangle the relationship among metformin, GDF15, and energy balance.
MeSH term(s)	Animals ; Glial Cell Line-Derived Neurotrophic Factor Receptors/metabolism ; Growth Differentiation Factor 15/metabolism ; Humans ; Metformin/pharmacology ; Metformin/therapeutic use ; Mice ; Obesity/metabolism ; Weight Loss
Chemical Substances	GDF15 protein, human ; GFRAL protein, mouse ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Growth Differentiation Factor 15 ; Metformin (9100L32L2N)
Language	English
Publishing date	2022-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.111258
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Article ; Online: ApoA-1 improves glucose tolerance by increasing glucose uptake into heart and skeletal muscle independently of AMPKα

Fritzen, Andreas Mæchel / Domingo-Espín, Joan / Lundsgaard, Anne-Marie / Kleinert, Maximilian / Israelsen, Ida / Carl, Christian S / Nicolaisen, Trine S / Kjøbsted, Rasmus / Jeppesen, Jacob F / Wojtaszewski, Jørgen F P / Lagerstedt, Jens O / Kiens, Bente

Molecular metabolism

2020 Volume 35, Page(s) 100949

Abstract: Objective: Acute administration of the main protein component of high-density lipoprotein, apolipoprotein A-I (ApoA-1), improves glucose uptake in skeletal muscle. The molecular mechanisms mediating this are not known, but in muscle cell cultures, ApoA- ... ...

Abstract	Objective: Acute administration of the main protein component of high-density lipoprotein, apolipoprotein A-I (ApoA-1), improves glucose uptake in skeletal muscle. The molecular mechanisms mediating this are not known, but in muscle cell cultures, ApoA-1 failed to increase glucose uptake when infected with a dominant-negative AMP-activated protein kinase (AMPK) virus. We therefore investigated whether AMPK is necessary for ApoA-1-stimulated glucose uptake in intact heart and skeletal muscle in vivo. Methods: The effect of injection with recombinant human ApoA-1 (rApoA-1) on glucose tolerance, glucose-stimulated insulin secretion, and glucose uptake into skeletal and heart muscle with and without block of insulin secretion by injection of epinephrine (0.1 mg/kg) and propranolol (5 mg/kg), were investigated in 8 weeks high-fat diet-fed (60E%) wild-type and AMPKα Results: rApoA-1 lowered plasma glucose concentration by 1.7 mmol/l within 3 h (6.1 vs 4.4 mmol/l; p < 0.001). Three hours after rApoA-1 injection, glucose tolerance during a 40-min glucose tolerance test (GTT) was improved compared to control (area under the curve (AUC) reduced by 45%, p < 0.001). This was accompanied by an increased glucose clearance into skeletal (+110%; p < 0.001) and heart muscle (+100%; p < 0.001) and an increase in glucose-stimulated insulin secretion 20 min after glucose injection (+180%; p < 0.001). When insulin secretion was blocked during a GTT, rApoA-1 still enhanced glucose tolerance (AUC lowered by 20% compared to control; p < 0.001) and increased glucose clearance into skeletal (+50%; p < 0.05) and heart muscle (+270%; p < 0.001). These improvements occurred to a similar extent in both wild-type and AMPKα Conclusions: In conclusion, ApoA-1 stimulates in vivo glucose disposal into skeletal and heart muscle independently of AMPKα
MeSH term(s)	AMP-Activated Protein Kinases/genetics ; AMP-Activated Protein Kinases/metabolism ; Animals ; Apolipoprotein A-I/administration & dosage ; Blood Glucose/metabolism ; Diet, High-Fat ; Female ; Glucose Tolerance Test ; Insulin/metabolism ; Insulin Secretion/drug effects ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muscle, Skeletal/metabolism ; Myocardium/metabolism ; Recombinant Proteins/administration & dosage ; Signal Transduction/drug effects
Chemical Substances	APOA1 protein, human ; Apolipoprotein A-I ; Blood Glucose ; Insulin ; Recombinant Proteins ; AMPK alpha2 subunit, mouse (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2020-03-04
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2020.01.013
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Article ; Online: Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure.

Nicolaisen, Trine S / Klein, Anders B / Dmytriyeva, Oksana / Lund, Jens / Ingerslev, Lars R / Fritzen, Andreas M / Carl, Christian S / Lundsgaard, Anne-Marie / Frost, Mikkel / Ma, Tao / Schjerling, Peter / Gerhart-Hines, Zachary / Flamant, Frederic / Gauthier, Karine / Larsen, Steen / Richter, Erik A / Kiens, Bente / Clemmensen, Christoffer

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2020 Volume 34, Issue 11, Page(s) 15480–15491

Abstract: Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered a key site for thyroid action, the contribution of thyroid hormone receptor signaling in muscle to whole-body energy ... ...

Abstract	Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered a key site for thyroid action, the contribution of thyroid hormone receptor signaling in muscle to whole-body energy metabolism and body temperature has not been resolved. Here, we show that T3-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRα
MeSH term(s)	Animals ; Energy Metabolism/drug effects ; Male ; Mice ; Mice, Knockout ; Muscle Fibers, Fast-Twitch/cytology ; Muscle Fibers, Fast-Twitch/drug effects ; Muscle Fibers, Fast-Twitch/physiology ; Muscle Fibers, Slow-Twitch/cytology ; Muscle Fibers, Slow-Twitch/drug effects ; Muscle Fibers, Slow-Twitch/physiology ; Muscle, Skeletal/cytology ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/physiology ; Physical Conditioning, Animal ; Thyroid Hormone Receptors alpha/physiology ; Thyroid Hormones/pharmacology ; Transcriptome
Chemical Substances	Thyroid Hormone Receptors alpha ; Thyroid Hormones
Language	English
Publishing date	2020-09-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202001258RR
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Pharmacological targeting of α3β4 nicotinic receptors improves peripheral insulin sensitivity in mice with diet-induced obesity.

Jall, Sigrid / De Angelis, Meri / Lundsgaard, Anne-Marie / Fritzen, Andreas M / Nicolaisen, Trine S / Klein, Anders B / Novikoff, Aaron / Sachs, Stephan / Richter, Erik A / Kiens, Bente / Schramm, Karl-Werner / Tschöp, Matthias H / Stemmer, Kerstin / Clemmensen, Christoffer / Müller, Timo D / Kleinert, Maximilian

Diabetologia

2020 Volume 63, Issue 6, Page(s) 1236–1247

Abstract: Aims/hypothesis: Treatment with the α3β4 nicotinic acetylcholine receptor (nAChR) agonist, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), improves glucose tolerance in diet-induced obese (DIO) mice, but the physiological and molecular mechanisms are ... ...

Abstract	Aims/hypothesis: Treatment with the α3β4 nicotinic acetylcholine receptor (nAChR) agonist, 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), improves glucose tolerance in diet-induced obese (DIO) mice, but the physiological and molecular mechanisms are unknown. Methods: DMPP (10 mg/kg body weight, s.c.) was administered either in a single injection (acute) or daily for up to 14 days (chronic) in DIO wild-type (WT) and Chrnb4 knockout (KO) mice and glucose tolerance, tissue-specific tracer-based glucose metabolism, and insulin signalling were assessed. Results: In WT mice, but not in Chrnb4 KO mice, single acute treatment with DMPP induced transient hyperglycaemia, which was accompanied by high plasma adrenaline (epinephrine) levels, upregulated hepatic gluconeogenic genes, and decreased hepatic glycogen content. In contrast to these acute effects, chronic DMPP treatment in WT mice elicited improvements in glucose tolerance already evident after three consecutive days of DMPP treatment. After seven days of DMPP treatment, glucose tolerance was markedly improved, also in comparison with mice that were pair-fed to DMPP-treated mice. The glycaemic benefit of chronic DMPP was absent in Chrnb4 KO mice. Chronic DMPP increased insulin-stimulated glucose clearance into brown adipose tissue (+69%), heart (+93%), gastrocnemius muscle (+74%) and quadriceps muscle (+59%), with no effect in white adipose tissues. After chronic DMPP treatment, plasma adrenaline levels did not increase following an injection with DMPP. In glucose-stimulated skeletal muscle, we detected a decreased phosphorylation of the inhibitory Ser640 phosphorylation site on glycogen synthase and a congruent increase in glycogen accumulation following chronic DMPP treatment. Conclusions/interpretation: Our data suggest that DMPP acutely induces adrenaline release and hepatic glycogenolysis, while chronic DMPP-mediated activation of β4-containing nAChRs improves peripheral insulin sensitivity independently of changes in body weight via mechanisms that could involve increased non-oxidative glucose disposal into skeletal muscle.
MeSH term(s)	Animals ; Blood Glucose/drug effects ; Catecholamines/metabolism ; Dimethylphenylpiperazinium Iodide/therapeutic use ; Hyperglycemia/drug therapy ; Hyperglycemia/metabolism ; Insulin Resistance/physiology ; Male ; Mice ; Mice, Knockout ; Nicotinic Agonists/therapeutic use ; Obesity/drug therapy ; Obesity/metabolism ; Receptors, Nicotinic/metabolism
Chemical Substances	Blood Glucose ; Catecholamines ; Nicotinic Agonists ; Receptors, Nicotinic ; nicotinic receptor alpha3beta4 ; Dimethylphenylpiperazinium Iodide (54-77-3)
Language	English
Publishing date	2020-03-06
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1694-9
ISSN	1432-0428 ; 0012-186X
ISSN (online)	1432-0428
ISSN	0012-186X
DOI	10.1007/s00125-020-05117-4
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Article ; Online: Pharmacological but not physiological GDF15 suppresses feeding and the motivation to exercise.

Klein, Anders B / Nicolaisen, Trine S / Ørtenblad, Niels / Gejl, Kasper D / Jensen, Rasmus / Fritzen, Andreas M / Larsen, Emil L / Karstoft, Kristian / Poulsen, Henrik E / Morville, Thomas / Sahl, Ronni E / Helge, Jørn W / Lund, Jens / Falk, Sarah / Lyngbæk, Mark / Ellingsgaard, Helga / Pedersen, Bente K / Lu, Wei / Finan, Brian /

Jørgensen, Sebastian B / Seeley, Randy J / Kleinert, Maximilian / Kiens, Bente / Richter, Erik A / Clemmensen, Christoffer

Nature communications

2021 Volume 12, Issue 1, Page(s) 1041

Abstract: Growing evidence supports that pharmacological application of growth differentiation factor 15 (GDF15) suppresses appetite but also promotes sickness-like behaviors in rodents via GDNF family receptor α-like (GFRAL)-dependent mechanisms. Conversely, the ... ...

Abstract	Growing evidence supports that pharmacological application of growth differentiation factor 15 (GDF15) suppresses appetite but also promotes sickness-like behaviors in rodents via GDNF family receptor α-like (GFRAL)-dependent mechanisms. Conversely, the endogenous regulation of GDF15 and its physiological effects on energy homeostasis and behavior remain elusive. Here we show, in four independent human studies that prolonged endurance exercise increases circulating GDF15 to levels otherwise only observed in pathophysiological conditions. This exercise-induced increase can be recapitulated in mice and is accompanied by increased Gdf15 expression in the liver, skeletal muscle, and heart muscle. However, whereas pharmacological GDF15 inhibits appetite and suppresses voluntary running activity via GFRAL, the physiological induction of GDF15 by exercise does not. In summary, exercise-induced circulating GDF15 correlates with the duration of endurance exercise. Yet, higher GDF15 levels after exercise are not sufficient to evoke canonical pharmacological GDF15 effects on appetite or responsible for diminishing exercise motivation.
MeSH term(s)	Adult ; Animals ; Appetite Regulation/physiology ; Creatine Kinase/blood ; Creatine Kinase/genetics ; Exercise/physiology ; Feeding Behavior/physiology ; Gene Expression Regulation ; Glial Cell Line-Derived Neurotrophic Factor Receptors/deficiency ; Glial Cell Line-Derived Neurotrophic Factor Receptors/genetics ; Growth Differentiation Factor 15/blood ; Growth Differentiation Factor 15/genetics ; Growth Differentiation Factor 15/metabolism ; Humans ; Interleukin-10/blood ; Interleukin-10/genetics ; Interleukin-6/administration & dosage ; Leptin/blood ; Leptin/genetics ; Liver/drug effects ; Liver/metabolism ; Male ; Mice ; Mice, Knockout ; Motivation/physiology ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Myocardium/metabolism ; Physical Conditioning, Animal ; Physical Endurance/physiology ; Time Factors
Chemical Substances	GDF15 protein, human ; Gdf15 protein, mouse ; Glial Cell Line-Derived Neurotrophic Factor Receptors ; Growth Differentiation Factor 15 ; IL10 protein, human ; IL6 protein, human ; Interleukin-6 ; LEP protein, human ; Leptin ; Interleukin-10 (130068-27-8) ; Creatine Kinase (EC 2.7.3.2)
Language	English
Publishing date	2021-02-15
Publishing country	England
Document type	Journal Article ; Observational Study ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-21309-x
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Article ; Online: Glucometabolic consequences of acute and prolonged inhibition of fatty acid oxidation.

Lundsgaard, Anne-Marie / Fritzen, Andreas M / Nicolaisen, Trine S / Carl, Christian S / Sjøberg, Kim A / Raun, Steffen H / Klein, Anders B / Sanchez-Quant, Eva / Langer, Jakob / Ørskov, Cathrine / Clemmensen, Christoffer / Tschöp, Matthias H / Richter, Erik A / Kiens, Bente / Kleinert, Maximilian

Journal of lipid research

2019 Volume 61, Issue 1, Page(s) 10–19

Abstract: Excessive circulating FAs have been proposed to promote insulin resistance (IR) of glucose metabolism by increasing the oxidation of FAs over glucose. Therefore, inhibition of FA oxidation (FAOX) has been suggested to ameliorate IR. However, prolonged ... ...

Abstract	Excessive circulating FAs have been proposed to promote insulin resistance (IR) of glucose metabolism by increasing the oxidation of FAs over glucose. Therefore, inhibition of FA oxidation (FAOX) has been suggested to ameliorate IR. However, prolonged inhibition of FAOX would presumably cause lipid accumulation and thereby promote lipotoxicity. To understand the glycemic consequences of acute and prolonged FAOX inhibition, we treated mice with the carnitine palmitoyltransferase 1 (CPT-1) inhibitor, etomoxir (eto), in combination with short-term 45% high fat diet feeding to increase FA availability. Eto acutely increased glucose oxidation and peripheral glucose disposal, and lowered circulating glucose, but this was associated with increased circulating FAs and triacylglycerol accumulation in the liver and heart within hours. Several days of FAOX inhibition by daily eto administration induced hepatic steatosis and glucose intolerance, specific to CPT-1 inhibition by eto. Lower whole-body insulin sensitivity was accompanied by reduction in brown adipose tissue (BAT) uncoupling protein 1 (UCP1) protein content, diminished BAT glucose clearance, and increased hepatic glucose production. Collectively, these data suggest that pharmacological inhibition of FAOX is not a viable strategy to treat IR, and that sufficient rates of FAOX are required for maintaining liver and BAT metabolic function.
MeSH term(s)	Animals ; Diet, High-Fat ; Epoxy Compounds/administration & dosage ; Epoxy Compounds/pharmacology ; Fatty Acids/chemistry ; Fatty Acids/metabolism ; Glucose/metabolism ; Glucose Intolerance/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Oxidation-Reduction/drug effects
Chemical Substances	Epoxy Compounds ; Fatty Acids ; Glucose (IY9XDZ35W2) ; etomoxir (MSB3DD2XP6)
Language	English
Publishing date	2019-11-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80154-9
ISSN	1539-7262 ; 0022-2275
ISSN (online)	1539-7262
ISSN	0022-2275
DOI	10.1194/jlr.RA119000177
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Article ; Online: Mechanisms Preserving Insulin Action during High Dietary Fat Intake.

Lundsgaard, Anne-Marie / Holm, Jacob B / Sjøberg, Kim A / Bojsen-Møller, Kirstine N / Myrmel, Lene S / Fjære, Even / Jensen, Benjamin A H / Nicolaisen, Trine S / Hingst, Janne R / Hansen, Sine L / Doll, Sophia / Geyer, Philip E / Deshmukh, Atul S / Holst, Jens J / Madsen, Lise / Kristiansen, Karsten / Wojtaszewski, Jørgen F P / Richter, Erik A / Kiens, Bente

Cell metabolism

2018 Volume 29, Issue 1, Page(s) 229

Language	English
Publishing date	2018-05-10
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2018.10.002
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Article ; Online: Mechanisms Preserving Insulin Action during High Dietary Fat Intake.

Cell metabolism

2018 Volume 29, Issue 1, Page(s) 50–63.e4

Abstract: Prolonged intervention studies investigating molecular metabolism are necessary for a deeper understanding of dietary effects on health. Here we provide mechanistic information about metabolic adaptation to fat-rich diets. Healthy, slightly overweight ... ...

Abstract	Prolonged intervention studies investigating molecular metabolism are necessary for a deeper understanding of dietary effects on health. Here we provide mechanistic information about metabolic adaptation to fat-rich diets. Healthy, slightly overweight men ingested saturated or polyunsaturated fat-rich diets for 6 weeks during weight maintenance. Hyperinsulinemic clamps combined with leg balance technique revealed unchanged peripheral insulin sensitivity, independent of fatty acid type. Both diets increased fat oxidation potential in muscle. Hepatic insulin clearance increased, while glucose production, de novo lipogenesis, and plasma triacylglycerol decreased. High fat intake changed the plasma proteome in the immune-supporting direction and the gut microbiome displayed changes at taxonomical and functional level with polyunsaturated fatty acid (PUFA). In mice, eucaloric feeding of human PUFA and saturated fatty acid diets lowered hepatic triacylglycerol content compared with low-fat-fed control mice, and induced adaptations in the liver supportive of decreased gluconeogenesis and lipogenesis. Intake of fat-rich diets thus induces extensive metabolic adaptations enabling disposition of dietary fat without metabolic complications.
MeSH term(s)	Animals ; Blood Glucose ; Diet, High-Fat/methods ; Dietary Fats, Unsaturated/metabolism ; Fatty Acids/metabolism ; Gluconeogenesis ; Glucose/metabolism ; Healthy Volunteers ; Humans ; Insulin/blood ; Insulin Resistance ; Lipogenesis ; Liver/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Muscles/metabolism
Chemical Substances	Blood Glucose ; Dietary Fats, Unsaturated ; Fatty Acids ; Insulin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2018-09-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2018.08.022
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