Lipocalin-2 is an anorexigenic signal in primates.

Autor:	Petropoulou PI; Department of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, United States., Mosialou I; Department of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, United States., Shikhel S; Department of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, United States., Hao L; Department of Nutritional Sciences, Rutgers University, New Brunswick, United States., Panitsas K; Department of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, United States., Bisikirska B; Department of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, United States., Luo N; Department of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, United States., Bahna F; Department of Biochemistry and Molecular Biophysics, Columbia University, New York, United States., Kim J; Department of Radiology, Columbia University Medical Center, New York, United States., Carberry P; Department of Radiology, Columbia University Medical Center, New York, United States., Zanderigo F; Department of Psychiatry, Columbia University Medical Center, New York, United States.; Molecular Imaging and Neuropathology Area, New York State Psychiatric Institute, New York, United States., Simpson N; Department of Psychiatry, Columbia University Medical Center, New York, United States., Bakalian M; Department of Psychiatry, Columbia University Medical Center, New York, United States., Kassir S; Department of Psychiatry, Columbia University Medical Center, New York, United States.; Molecular Imaging and Neuropathology Area, New York State Psychiatric Institute, New York, United States., Shapiro L; Department of Biochemistry and Molecular Biophysics, Columbia University, New York, United States., Underwood MD; Department of Psychiatry, Columbia University Medical Center, New York, United States.; Molecular Imaging and Neuropathology Area, New York State Psychiatric Institute, New York, United States., May CM; Department of Pathology, Section on Comparative Medicine, Wake Forest School of Medicine, Winston-Salem, United States., Soligapuram Sai KK; Department of Radiology, Wake Forest School of Medicine, Winston-Salem, United States., Jorgensen MJ; Department of Pathology, Section on Comparative Medicine, Wake Forest School of Medicine, Winston-Salem, United States., Confavreux CB; INSERM UMR1033-Université de Lyon-Hospices Civils de Lyon, Lyon, France., Shapses S; Department of Nutritional Sciences, Rutgers University, New Brunswick, United States.; Department of Medicine, Rutgers - RWJ Medical School, Rutgers University, New Brunswick, United States., Laferrère B; New York Obesity Nutrition Research Center, Columbia University, New York, United States.; Department of Medicine, Division of Endocrinology, Columbia University Irving Medical Center, New York, United States., Mintz A; Department of Radiology, Columbia University Medical Center, New York, United States., Mann JJ; Department of Radiology, Columbia University Medical Center, New York, United States.; Department of Psychiatry, Columbia University Medical Center, New York, United States.; Molecular Imaging and Neuropathology Area, New York State Psychiatric Institute, New York, United States., Rubin M; New York Obesity Nutrition Research Center, Columbia University, New York, United States., Kousteni S; Department of Physiology and Cellular Biophysics, Columbia University Medical Center, New York, United States.
Jazyk:	angličtina
Zdroj:	ELife [Elife] 2020 Nov 24; Vol. 9. Date of Electronic Publication: 2020 Nov 24.
DOI:	10.7554/eLife.58949
Abstrakt:	In the mouse, the osteoblast-derived hormone Lipocalin-2 (LCN2) suppresses food intake and acts as a satiety signal. We show here that meal challenges increase serum LCN2 levels in persons with normal or overweight, but not in individuals with obesity. Postprandial LCN2 serum levels correlate inversely with hunger sensation in challenged subjects. We further show through brain PET scans of monkeys injected with radiolabeled recombinant human LCN2 (rh-LCN2) and autoradiography in baboon, macaque, and human brain sections, that LCN2 crosses the blood-brain barrier and localizes to the hypothalamus in primates. In addition, daily treatment of lean monkeys with rh-LCN2 decreases food intake by 21%, without overt side effects. These studies demonstrate the biology of LCN2 as a satiety factor and indicator and anorexigenic signal in primates. Failure to stimulate postprandial LCN2 in individuals with obesity may contribute to metabolic dysregulation, suggesting that LCN2 may be a novel target for obesity treatment. Competing Interests: PP, IM, SS, LH, KP, BB, NL, FB, JK, PC, FZ, NS, MB, SK, LS, MU, CM, KS, MJ, CC, SS, BL, AM, JM, MR, SK No competing interests declared (© 2020, Petropoulou et al.)
Databáze:	MEDLINE
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