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3. Neuronal loss of TRPM8 leads to obesity and glucose intolerance in male mice

Author

Liskiewicz, D., Zhang, Q., Barthem, Clarissa S., Jastroch, Martin, Liskiewicz, A., Khajavi, N., Grandl, G., Coupland, C., Kleinert, M., Garcia-Caceres, C., Novikoff, A., Maity, G., Boehm, U., Tschöp, M. H., Müller, T. D., Liskiewicz, D., Zhang, Q., Barthem, Clarissa S., Jastroch, Martin, Liskiewicz, A., Khajavi, N., Grandl, G., Coupland, C., Kleinert, M., Garcia-Caceres, C., Novikoff, A., Maity, G., Boehm, U., Tschöp, M. H., and Müller, T. D.

Abstract

Objective: Mice with global deletion of the transient receptor potential channel melastatin family member 8 (TRPM8) are obese, and treatment of diet-induced obese (DIO) mice with TRPM8 agonists decrease body weight. Whether TRPM8 signaling regulates energy metabolism via central or peripheral effects is unknow. Here we assessed the metabolic phenotype of mice with either Nestin Cre-mediated neuronal loss of TRPM8, or with deletion of TRPM8 in Advillin Cre positive sensory neurons of the peripheral nervous system (PNS). Methods: Nestin Cre- and Advillin Cre-Trpm8 knock-out (KO) mice were metabolically phenotyped under chronic exposure to either chow or high-fat diet (HFD), followed by assessment of energy and glucose metabolism. Results: At room temperature, chow-fed neuronal Trpm8 KO are obese and show decreased energy expenditure when acutely treated with the TRPM8 selective agonist icilin. But body weight of neuronal Trpm8 KO mice is indistinguishable from wildtype controls at thermoneutrality, or when mice are chronically exposed to HFD-feeding. In contrast to previous studies, we show that the TRPM8 agonist icilin has no direct effect on brown adipocytes, but that icilin stimulates energy expenditure, at least in part, via neuronal TRPM8 signaling. We further show that lack of TRPM8 in sensory neurons of the PNS does not lead to a metabolically relevant phenotype. Conclusions: Our data indicate that obesity in TRPM8-deficient mice is centrally mediated and likely originates from alterations in energy expenditure and/or thermal conductance, but does not depend on TRPM8 signaling in brown adipocytes or sensory neurons of the PVN.

Published
2023
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5. Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index

Author

Hinney, A, Kesselmeier, M, Jall, S, Volckmar, A-L, Föcker, M, Antel, J, Heid, I M, Winkler, T W, Grant, S F A, Guo, Y, Bergen, A W, Kaye, W, Berrettini, W, Hakonarson, H, Herpertz-Dahlmann, B, de Zwaan, M, Herzog, W, Ehrlich, S, Zipfel, S, Egberts, K M, Adan, R, Brandys, M, van Elburg, A, Boraska Perica, V, Franklin, C S, Tschöp, M H, Zeggini, E, Bulik, C M, Collier, D, Scherag, A, Müller, T D, and Hebebrand, J

Published
2017
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10. Erratum: Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index

Author

Hinney, A, Kesselmeier, M, Jall, S, Volckmar, A-L, Föcker, M, Antel, J, Heid, I M, Winkler, T W, Guo, Y, Bergen, A W, Kaye, W, Berrettini, W, Hakonarson, H, Herpertz-Dahlmann, B, de Zwaan, M, Herzog, W, Ehrlich, S, Zipfel, S, Egberts, K M, Adan, R, Brandys, M, van Elburg, A, Boraska Perica, V, Franklin, C S, Tschöp, M H, Zeggini, E, Bulik, C M, Collier, D, Scherag, A, Müller, T D, and Hebebrand, J

Published
2017
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27. PYY3-36 as an anti-obesity drug target

Author

Boggiano, M. M., Chandler, P. C., Oswald, K. D., Rodgers, R. J., Blundell, J. E., Ishii, Y., Beattie, A. H., Holch, P., Allison, D. B., Schindler, M., Arndt, K., Rudolf, K., Mark, M., Schoelch, C., Joost, H. G., Klaus, S., Thöne-Reineke, C., Benoit, S. C., Seeley, R. J., Beck-Sickinger, A. G., Koglin, N., Raun, K., Madsen, K., Wulff, B. S., Stidsen, C. E., Birringer, M., Kreuzer, O. J., Deng, X. Y., Whitcomb, D. C., Halem, H., Taylor, J., Dong, J., Datta, R., Culler, M., Ortmann, S., Castañeda, T. R., and Tschöp, M.

Published
2005

29. Physiology: Does gut hormone PYY3-36 decrease food intake in rodents?

Author

Tschöp, M., Castañeda, T. R., Joost, H. G., Thöne-Reineke, C., Ortmann, S., Klaus, S., Hagan, M. M., Chandler, P. C., Oswald, K. D., Benoit, S. C., Seeley, R. J., Kinzig, K. P., Moran, T. H., Beck-Sickinger, A. G., Koglin, N., Rodgers, R. J., Blundell, J. E., Ishii, Y., Beattie, A. H., Holch, P., Allison, D. B., Raun, K., Madsen, K., Wulff, B. S., Stidsen, C. E., Birringer, M., Kreuzer, O. J., Schindler, M., Arndt, K., Rudolf, K., Mark, M., Deng, X. Y., Withcomb, D. C., Halem, H., Taylor, J., Dong, J., Datta, R., Culler, M., Craney, S., Flora, D., Smiley, D., and Heiman, M. L.

Published
2004

36. Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index

Author

Experimental psychopathology, Leerstoel Elburg, Hinney, A, Kesselmeier, M, Jall, S, Volckmar, A-L, Föcker, M, Antel, J, Heid, I M, Winkler, T W, Grant, S F A, Guo, Y, Bergen, A W, Kaye, W, Berrettini, W, Hakonarson, H, Herpertz-Dahlmann, B, de Zwaan, M, Herzog, W, Ehrlich, S, Zipfel, S, Egberts, K M, Adan, R, Brandys, M, van Elburg, A, Boraska Perica, V, Franklin, C S, Tschöp, M H, Zeggini, E, Bulik, C M, Collier, D, Scherag, A, Müller, T D, Hebebrand, J, GCAN, Experimental psychopathology, Leerstoel Elburg, Hinney, A, Kesselmeier, M, Jall, S, Volckmar, A-L, Föcker, M, Antel, J, Heid, I M, Winkler, T W, Grant, S F A, Guo, Y, Bergen, A W, Kaye, W, Berrettini, W, Hakonarson, H, Herpertz-Dahlmann, B, de Zwaan, M, Herzog, W, Ehrlich, S, Zipfel, S, Egberts, K M, Adan, R, Brandys, M, van Elburg, A, Boraska Perica, V, Franklin, C S, Tschöp, M H, Zeggini, E, Bulik, C M, Collier, D, Scherag, A, Müller, T D, Hebebrand, J, and GCAN

Published
2017

37. Geschichte der intravenösen Anästhesie

Author

Tschöp, M., Weis, K. H., Bergmann, H., editor, Brückner, J. B., editor, Gemperle, G., editor, Henschel, W. F., editor, Mayrhofer, O., editor, Meßmer, K., editor, Peter, K., editor, and Zinganell, Klaus, editor

Published
1987
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38. Megaloblastäre Anämie durch Fehlernährung

Author

Tschöp M, Folwaczny C, Loeschke K, and Schindlbeck N

Subjects
medicine.medical_specialty, Malabsorption, medicine.diagnostic_test, business.industry, Sinus tachycardia, Physical examination, General Medicine, medicine.disease, Gastroenterology, Folic acid, Schilling test, Internal medicine, Medicine, Alcohol intake, Vitamin B12, medicine.symptom, business, Exocrine pancreatic insufficiency
Abstract

HISTORY AND CLINICAL FINDINGS Over a period of about 6 weeks a 49-year-old woman developed increasing exercise-dependent dyspnoea. Her general practitioner had diagnosed marked megaloblastic anaemia and she was hospitalised for its further elucidation. She reported to have eaten or drunk nothing but sweets, potato chips, salty pretzels, lemonade, coffee and tea over the last 2 years. Alcohol intake had been reliably denied by her and outsiders. On admission she weighed 106 kg, her height was 167 cm, and she looked anaemic, had dyspnoea and a sinus tachycardia. There was no evidence of external or internal bleeding and the physical examination was otherwise unremarkable. INVESTIGATIONS Laboratory tests showed a haemoglobin concentration of 4.7 g/dl, as well as marked folic and vitamin B12 deficiency. The food items taken by her contain practically no cobalamine and no folic acid. Gastroscopy revealed grade 1 reflux oesophagitis. Malabsorption being excluded (normal Schilling test, no demonstrable autoantibodies against parietal cells, no evidence of exocrine pancreatic insufficiency), the lack of both vitamins and the megaloblastic anaemia caused by it could be explained only by a deficient food intake over several years. TREATMENT AND COURSE After administration of cobalamine (1 mg intramuscularly twice weekly for 6 weeks, then 300 micrograms daily by mouth for 4 weeks) and folic acid (5 mg twice daily for 10 weeks), as well as a well-balanced diet as prescribed by a dietician, reticulocyte and erythrocyte concentrations had quickly risen to normal at a follow-up examination 2 months later. CONCLUSION The case of an anaemia entirely caused by a deficient diet dearly illustrates the need of a well-balanced food intake even in adults.

Published
2008

41. miR-184 regulates pancreatic β-cell function according to glucose metabolism

Author

Tattikota, S.G., Rathjen, T., Hausser, J., Khedkar, A., Kabra, U.D., Pandey, V.K., Sury, M.D., Wessels, H.H., Mollet, I.G., Eliasson, L., Selbach, M., Zinzen, R.P., Zavolan, M., Kadener, S., Tschöp, M., Jastroch, M., Friedländer, M.R., and Poy, M.N.

Subjects
Cancer Research, Cardiovascular and Metabolic Diseases, Function and Dysfunction of the Nervous System
Abstract

In response to fasting or hyperglycemia, the pancreatic {beta}-cell alters its output of secreted insulin; however the pathways governing this adaptive response are not entirely established. While the precise role of microRNAs (miRNAs) is also unclear, a recurring theme emphasizes their function in cellular stress responses. We recently showed that miR-184, an abundant miRNA in the {beta}-cell, regulates compensatory proliferation and secretion during insulin resistance. Consistent with previous studies showing miR-184 suppresses insulin release, expression of this miRNA was increased in islets after fasting, demonstrating an active role in the {beta}-cell as glucose levels lower and the insulin demand ceases. Additionally, miR-184 was negatively regulated upon administration of a sucrose-rich diet in Drosophila demonstrating strong conservation of this pathway through evolution. Furthermore, miR-184 and its target Argonaute2 (Ago2) remained inversely correlated as concentrations of extracellular glucose increased, underlining a functional relationship between this miRNA and its targets. Lastly, restoration of Ago2 in the presence of miR-184 rescued suppression of miR-375-targeted genes suggesting these genes act in a coordinated manner during changes in the metabolic context. Together, these results highlight the adaptive role of miR-184 according to glucose metabolism and suggest the regulatory role of this miRNA in energy homeostasis is highly conserved.

Published
2015

43. Ghrelin modulates encoding-related brain function without enhancing memory formation in humans

Author

Kunath, N., primary, Müller, N.C.J., additional, Tonon, M., additional, Konrad, B.N., additional, Pawlowski, M., additional, Kopczak, A., additional, Elbau, I., additional, Uhr, M., additional, Kühn, S., additional, Repantis, D., additional, Ohla, K., additional, Müller, T.D., additional, Fernández, G., additional, Tschöp, M., additional, Czisch, M., additional, Steiger, A., additional, and Dresler, M., additional

Published
2016
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44. Ghrelin

Author

Müller, T D, Nogueiras, R, Andermann, M L, Andrews, Z B, Anker, S D, Argente, J, Batterham, R L, Benoit, S C, Bowers, C Y, Broglio, F, Casanueva, F F, D'Alessio, D, Depoortere, I, Geliebter, A, Ghigo, E, Cole, P A, Cowley, M, Cummings, D E, Dagher, A, Diano, S, Dickson, S L, Diéguez, C, Granata, R, Grill, H J, Grove, K, Habegger, K M, Heppner, K, Heiman, M L, Holsen, L, Holst, B, Inui, A, Jansson, J O, Kirchner, H, Korbonits, M, Laferrère, B, LeRoux, C W, Lopez, M, Morin, S, Nakazato, M, Nass, R, Perez-Tilve, D, Pfluger, P T, Schwartz, T W, Seeley, R J, Sleeman, M, Sun, Y, Sussel, L, Tong, J, Thorner, M O, van der Lely, A J, van der Ploeg, L H T, Zigman, J M, Kojima, M, Kangawa, K, Smith, R G, Horvath, T, and Tschöp, M H

Subjects
Growth hormone segretagogue receptor, Ghrelin
Abstract

The gastrointestinal peptide hormone ghrelin was discovered in 1999 as the endogenous ligand of the growth hormone secretagogue receptor. Increasing evidence supports more complicated and nuanced roles for the hormone, which go beyond the regulation of systemic energy metabolism.

Published
2015

46. Berufspolitik BDU, Heft 9/03

Author

Ristow M, S. Anker, Wiebke Arlt, and Tschöp M

Subjects
Medical education, business.industry, Urology, Medicine, business
Published
2003

49. A history of obesity leaves an inflammatory fingerprint in liver and adipose tissue

Author

Fischer, I P, Irmler, M, Meyer, C W, Sachs, S J, Neff, F, Hrabe de Angelis, M, Beckers, J, Tschöp, M H, Hofmann, S M, and Ussar, S

Abstract

Background/Objectives:Dieting is a popular yet often ineffective way to lower body weight, as the majority of people regain most of their pre-dieting weights in a relatively short time. The underlying molecular mechanisms driving weight regain and the increased risk for metabolic disease are still incompletely understood. Here we investigate the molecular alterations inherited from a history of obesity.Methods:In our model, male high-fat diet (HFD)-fed obese C57BL/6J mice were switched to a low caloric chow diet, resulting in a decline of body weight to that of lean mice. We measured body composition, as well as metrics of glucose, insulin and lipid homeostasis. This was accompanied by histological and gene expression analysis of adipose tissue and liver to assess adipose tissue inflammation and hepatosteatosis. Moreover, acute hypothalamic response to (re-) exposure to HFD was assessed by qPCR.Results & Conclusions:Within 7 weeks after diet switch, most obesity-associated phenotypes, such as body mass, glucose intolerance and blood metabolite levels were reversed. However, hepatic inflammation, hepatic steatosis as well as hypertrophy and inflammation of perigonadal, but not subcutaneous, adipocytes persisted in formerly obese mice. Transcriptional profiling of liver and perigonadal fat revealed an upregulation of pathways associated with immune function and cellularity. Thus, we show that weight reduction leaves signs of inflammation in liver and perigonadal fat, indicating that persisting proinflammatory signals in liver and adipose tissue could contribute to an increased risk of formerly obese subjects to develop the metabolic syndrome upon recurring weight gain.

Published
2018
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50. Ghrelin-induced hypothermia: A physiological basis but no clinical risk

Author

Wiedmer, P, Strasser, F, Horvath, T L, Blum, D, Dimarchi, R, Lutz, T, Schürmann, A, Joost, H G, Tschöp, M H, Tong, J, Wiedmer, P, Strasser, F, Horvath, T L, Blum, D, Dimarchi, R, Lutz, T, Schürmann, A, Joost, H G, Tschöp, M H, and Tong, J

Abstract

Ghrelin increases food intake and decreases energy expenditure, promoting a positive energy balance. We observed a single case of serious hypothermia during sustained ghrelin treatment in a male subject, suggesting that ghrelin may play a role in the regulation of body temperature. We therefore investigated the effect of ghrelin treatment on body temperature in rodents and humans under controlled conditions. Intriguingly, we could demonstrate ghrelin binding in axon terminals of the medial preoptic area of the hypothalamus located in the vicinity of cold-sensitive neurons. This localization of ghrelin receptors provides a potential anatomical basis for the regulation of body temperature by ghrelin. However, our follow-up studies also indicated that neither a chronic i.c.v. application of ghrelin in rats, nor a single s.c. injection under cold exposure in mice resulted in a relevant decrease in body core temperature. In addition, a four-hour intravenous ghrelin infusion did not decrease body surface temperature in healthy humans. We concluded that while there is a theoretical molecular basis for ghrelin to modify body temperature in mammals, its magnitude is irrelevant under physiologic circumstances. Hypothermia is not likely to represent a serious risk associated with this agent and pathway.

Published
2011

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