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Article: Central Feminization of Obese Male Mice Reduces Metabolic Syndrome.

Blackmore, Katherine / Young, Colin N

2022 Volume 12, Issue 10

Abstract: Metabolic syndrome encompasses a spectrum of conditions that increases the risk for cardiovascular and metabolic diseases. It is widely accepted that the sex hormone estrogen plays a protective metabolic role in premenopausal women, in part through ... ...

Abstract	Metabolic syndrome encompasses a spectrum of conditions that increases the risk for cardiovascular and metabolic diseases. It is widely accepted that the sex hormone estrogen plays a protective metabolic role in premenopausal women, in part through central nervous system (CNS) mechanisms. However, most work to date has focused on the loss of estrogen in females (e.g., menopause). Interestingly, transgender individuals receiving feminizing gender affirming therapy (i.e., estrogen) are relatively protected from metabolic syndrome conditions, pointing to a role for CNS estrogen in the development of metabolic syndrome in men. Here, we show that estrogen signaling in the brain protects males from metabolic syndrome and obesity related complications. First, short-term CNS specific supplementation of low-dose 17-β-estradiol in diet-induced obese male mice resulted in a significant reduction in body weight in parallel with a decrease in food intake without alterations in energy expenditure. In conjunction, central supplementation of estrogen reduced visceral adiposity, including epididymal and abdominal regions, with slighter decreases in subcutaneous inguinal and thermogenic brown adipose tissue. Furthermore, central estrogen administration reduced the liver manifestation of metabolic syndrome including hepatomegaly and hepatic steatosis. Collectively, these findings indicate that a lack of estrogen action in the brain may predispose males to metabolic syndrome pathogenesis.
Language	English
Publishing date	2022-09-30
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci12101324
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Article ; Online: Large-field-of-view scanning electron microscopy of the paraventricular nucleus of the hypothalamus during diet-induced obesity.

Arestakesyan, Hovhannes / Blackmore, Katherine / Smith, Hannah C / Popratiloff, Anastas / Young, Colin N

Journal of neurophysiology

2023 Volume 130, Issue 2, Page(s) 345–352

Abstract: Dysregulation in the paraventricular nucleus of the hypothalamus (PVN) is associated with a variety of diseases including those related to obesity. Although most investigations have focused on molecular changes, structural alterations in PVN neurons can ... ...

Abstract	Dysregulation in the paraventricular nucleus of the hypothalamus (PVN) is associated with a variety of diseases including those related to obesity. Although most investigations have focused on molecular changes, structural alterations in PVN neurons can reveal underlying functional disruptions. Although electron microscopy (EM) can provide nanometer resolution of brain structures, an inherent limitation of traditional transmission EM is the single field of view nature of data collection. To overcome this, we used large-field-of-view high-resolution backscatter scanning electron microscopy (bSEM) of the PVN. By stitching high-resolution bSEM images, taken from normal chow and high-fat diet mice, we achieved interactive, zoomable maps that allow for low-magnification screening of the entire PVN and high-resolution analyses of ultrastructure at the level of the smallest cellular organelle. Using this approach, quantitative analysis across the PVN revealed marked electron-dense regions within neuronal nucleoplasm following high-fat diet feeding, with an increase in kurtosis, indicative of a shift away from a normal distribution. Furthermore, measures of skewness indicated a shift toward darker clustered electron-dense regions, potentially indicative of heterochromatin clusters. We further demonstrate the utility to map out healthy and altered neurons throughout the PVN and the ability to remotely perform bSEM imaging in situations that require social distancing, such as the COVID-19 pandemic. Collectively, these findings present an approach that allows for the precise placement of PVN cells within an overall structural and functional map of the PVN. Moreover, they suggest that obesity may disrupt PVN neuronal chromatin structure.
MeSH term(s)	Mice ; Animals ; Humans ; Paraventricular Hypothalamic Nucleus ; Microscopy, Electron, Scanning ; Pandemics ; COVID-19 ; Hypothalamus ; Obesity ; Diet, High-Fat/adverse effects
Language	English
Publishing date	2023-07-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80161-6
ISSN	1522-1598 ; 0022-3077
ISSN (online)	1522-1598
ISSN	0022-3077
DOI	10.1152/jn.00208.2023
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Article ; Online: LKB1-AMPK modulates nutrient-induced changes in the mode of division of intestinal epithelial crypt cells in mice.

Blackmore, Katherine / Zhou, Weinan / Dailey, Megan J

Experimental biology and medicine (Maywood, N.J.)

2017 Volume 242, Issue 15, Page(s) 1490–1498

Abstract: Nutrient availability influences intestinal epithelial stem cell proliferation and tissue growth. Increases in food result in a greater number of epithelial cells, villi height and crypt depth. We investigated whether this nutrient-driven expansion of ... ...

Abstract	Nutrient availability influences intestinal epithelial stem cell proliferation and tissue growth. Increases in food result in a greater number of epithelial cells, villi height and crypt depth. We investigated whether this nutrient-driven expansion of the tissue is the result of a change in the mode of intestinal epithelial stem cell division and if LKB1-AMPK signaling plays a role. We utilized in vivo and in vitro experiments to test this hypothesis. C57BL/6J mice were separated into four groups and fed varying amounts of chow for 18 h: (1) ad libitum, (2) 50% of their average daily intake (3) fasted or (4) fasted for 12 h and refed. Mice were sacrificed, intestinal sections excised and immunohistochemically processed to determine the mitotic spindle orientation. Epithelial organoids in vitro were treated with no (0 mM), low (5 mM) or high (20 mM) amounts of glucose with or without an activator (Metformin) or inhibitor (Compound C) of LKB1-AMPK signaling. Cells were then processed to determine the mode of stem cell division. Fasted mice show a greater % of asymmetrically dividing cells compared with the other feeding groups. Organoids incubated with 0 mM glucose resulted in a greater % of asymmetrically dividing cells compared with the low or high-glucose conditions. In addition, LKB1-AMPK activation attenuated the % of symmetric division normally seen in high-glucose conditions. In contrast, LKB1-AMPK inhibition attenuated the % of asymmetric division normally seen in no glucose conditions. These data suggest that nutrient availability dictates the mode of division and that LKB1-AMPK mediates this nutrient-driven effect on intestinal epithelial stem cell proliferation. Impact statement The underlying cell biology of changes in the polarity of mitotic spindles and its relevance to tissue growth is a new concept and, thus, these data provide novel findings to begin to explain how this process contributes to the regeneration and growth of tissues. We find that short-term changes in food intake in vivo or glucose availability in vitro dictate the mode of division of crypt cells. In addition, we find that LKB1-AMPK signaling modulates the glucose-induced changes in the mode of division in vitro. Identifying mechanisms involved in the mode of division may provide new targets to control tissue growth.
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; Animals ; Cell Division ; Cell Proliferation ; Epithelial Cells/physiology ; Food ; Immunohistochemistry ; Intestinal Mucosa/cytology ; Male ; Mice, Inbred C57BL ; Organoids ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Stem Cells/physiology
Chemical Substances	Stk11 protein, mouse (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2017-08-02
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	4015-0
ISSN	1535-3699 ; 1525-1373 ; 0037-9727
ISSN (online)	1535-3699 ; 1525-1373
ISSN	0037-9727
DOI	10.1177/1535370217724427
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Article ; Online: A forebrain-hypothalamic ER stress driven circuit mediates hepatic steatosis during obesity.

Blackmore, Katherine / Houchen, Claire J / Simonyan, Hayk / Arestakesyan, Hovhannes / Stark, Alyssa K / Dow, Samantha A / Kim, Han Rae / Jeong, Jin Kwon / Popratiloff, Anastas / Young, Colin N

Molecular metabolism

2023 Volume 79, Page(s) 101858

Abstract: Objective: Non-alcoholic fatty liver disease (NAFLD) affects 1 in 3 adults and contributes to advanced liver injury and cardiometabolic disease. While recent evidence points to involvement of the brain in NAFLD, the downstream neural circuits and ... ...

Abstract	Objective: Non-alcoholic fatty liver disease (NAFLD) affects 1 in 3 adults and contributes to advanced liver injury and cardiometabolic disease. While recent evidence points to involvement of the brain in NAFLD, the downstream neural circuits and neuronal molecular mechanisms involved in this response, remain unclear. Here, we investigated the role of a unique forebrain-hypothalamic circuit in NAFLD. Methods: Chemogenetic activation and inhibition of circumventricular subfornical organ (SFO) neurons that project to the paraventricular nucleus of the hypothalamus (PVN; SFO→PVN) in mice were used to study the role of SFO→PVN signaling in NAFLD. Novel scanning electron microscopy techniques, histological approaches, molecular biology techniques, and viral methodologies were further used to delineate the role of endoplasmic reticulum (ER) stress within this circuit in driving NAFLD. Results: In lean animals, acute chemogenetic activation of SFO→PVN neurons was sufficient to cause hepatic steatosis in a liver sympathetic nerve dependent manner. Conversely, inhibition of this forebrain-hypothalamic circuit rescued obesity-associated NAFLD. Furthermore, dietary NAFLD is associated with marked ER ultrastructural alterations and ER stress in the PVN, which was blunted following reductions in excitatory signaling from the SFO. Finally, selective inhibition of PVN ER stress reduced hepatic steatosis during obesity. Conclusions: Collectively, these findings characterize a previously unrecognized forebrain-hypothalamic-ER stress circuit that is involved in hepatic steatosis, which may point to future therapeutic strategies for NAFLD.
MeSH term(s)	Mice ; Animals ; Non-alcoholic Fatty Liver Disease ; Obesity ; Paraventricular Hypothalamic Nucleus/physiology ; Sympathetic Nervous System
Language	English
Publishing date	2023-12-21
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2708735-9
ISSN	2212-8778 ; 2212-8778
ISSN (online)	2212-8778
ISSN	2212-8778
DOI	10.1016/j.molmet.2023.101858
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Article: LKB1-AMPK modulates nutrient-induced changes in the mode of division of intestinal epithelial crypt cells in mice

Blackmore, Katherine / Zhou, Weinan / Dailey, Megan J.

Experimental Biology and Medicine. 2019 Sept., v. 242, no. 15

2017

Abstract	Nutrient availability influences intestinal epithelial stem cell proliferation and tissue growth. Increases in food result in a greater number of epithelial cells, villi height and crypt depth. We investigated whether this nutrient-driven expansion of the tissue is the result of a change in the mode of intestinal epithelial stem cell division and if LKB1-AMPK signaling plays a role. We utilized in vivo and in vitro experiments to test this hypothesis. C57BL/6J mice were separated into four groups and fed varying amounts of chow for 18 h: (1) ad libitum, (2) 50% of their average daily intake (3) fasted or (4) fasted for 12 h and refed. Mice were sacrificed, intestinal sections excised and immunohistochemically processed to determine the mitotic spindle orientation. Epithelial organoids in vitro were treated with no (0 mM), low (5 mM) or high (20 mM) amounts of glucose with or without an activator (Metformin) or inhibitor (Compound C) of LKB1-AMPK signaling. Cells were then processed to determine the mode of stem cell division. Fasted mice show a greater % of asymmetrically dividing cells compared with the other feeding groups. Organoids incubated with 0 mM glucose resulted in a greater % of asymmetrically dividing cells compared with the low or high-glucose conditions. In addition, LKB1-AMPK activation attenuated the % of symmetric division normally seen in high-glucose conditions. In contrast, LKB1-AMPK inhibition attenuated the % of asymmetric division normally seen in no glucose conditions. These data suggest that nutrient availability dictates the mode of division and that LKB1-AMPK mediates this nutrient-driven effect on intestinal epithelial stem cell proliferation. Impact statement The underlying cell biology of changes in the polarity of mitotic spindles and its relevance to tissue growth is a new concept and, thus, these data provide novel findings to begin to explain how this process contributes to the regeneration and growth of tissues. We find that short-term changes in food intake in vivo or glucose availability in vitro dictate the mode of division of crypt cells. In addition, we find that LKB1-AMPK signaling modulates the glucose-induced changes in the mode of division in vitro. Identifying mechanisms involved in the mode of division may provide new targets to control tissue growth.
Keywords	AMP-activated protein kinase ; ad libitum feeding ; animal models ; average daily intake ; cell division ; cell proliferation ; enzyme activation ; enzyme inhibition ; epithelial cells ; fasting ; food intake ; glucose ; immunohistochemistry ; intestinal crypts ; metformin ; mice ; mitotic spindle apparatus ; nutrient availability ; organoids ; refeeding ; signal transduction ; stem cells
Language	English
Dates of publication	2017-09
Size	p. 1490-1498.
Publishing place	SAGE Publications
Document type	Article
ISSN	1535-3702
DOI	10.1177/1535370217724427
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Article ; Online: Irisin acts through its integrin receptor in a two-step process involving extracellular Hsp90α.

Molecular cell

2024 Volume 83, Issue 11, Page(s) 1903–1920.e12

Abstract: Exercise benefits the human body in many ways. Irisin is secreted by muscle, increased with exercise, and conveys physiological benefits, including improved cognition and resistance to neurodegeneration. Irisin acts via αV integrins; however, a ... ...

Abstract	Exercise benefits the human body in many ways. Irisin is secreted by muscle, increased with exercise, and conveys physiological benefits, including improved cognition and resistance to neurodegeneration. Irisin acts via αV integrins; however, a mechanistic understanding of how small polypeptides like irisin can signal through integrins is poorly understood. Using mass spectrometry and cryo-EM, we demonstrate that the extracellular heat shock protein 90α (eHsp90α) is secreted by muscle with exercise and activates integrin αVβ5. This allows for high-affinity irisin binding and signaling through an Hsp90α/αV/β5 complex. By including hydrogen/deuterium exchange data, we generate and experimentally validate a 2.98 Å RMSD irisin/αVβ5 complex docking model. Irisin binds very tightly to an alternative interface on αVβ5 distinct from that used by known ligands. These data elucidate a non-canonical mechanism by which a small polypeptide hormone like irisin can function through an integrin receptor.
MeSH term(s)	Humans ; Fibronectins/metabolism ; Cell Communication ; Signal Transduction
Chemical Substances	Fibronectins
Language	English
Publishing date	2024-01-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2023.05.008
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Article ; Online: Isolation of extracellular fluids reveals novel secreted bioactive proteins from muscle and fat tissues.

Mittenbühler, Melanie J / Jedrychowski, Mark P / Van Vranken, Jonathan G / Sprenger, Hans-Georg / Wilensky, Sarah / Dumesic, Phillip A / Sun, Yizhi / Tartaglia, Andrea / Bogoslavski, Dina / A, Mu / Xiao, Haopeng / Blackmore, Katherine A / Reddy, Anita / Gygi, Steven P / Chouchani, Edward T / Spiegelman, Bruce M

Cell metabolism

2023 Volume 35, Issue 3, Page(s) 535–549.e7

Abstract: Proteins are secreted from cells to send information to neighboring cells or distant tissues. Because of the highly integrated nature of energy balance systems, there has been particular interest in myokines and adipokines. These are challenging to study ...

Abstract	Proteins are secreted from cells to send information to neighboring cells or distant tissues. Because of the highly integrated nature of energy balance systems, there has been particular interest in myokines and adipokines. These are challenging to study through proteomics because serum or plasma contains highly abundant proteins that limit the detection of proteins with lower abundance. We show here that extracellular fluid (EF) from muscle and fat tissues of mice shows a different protein composition than either serum or tissues. Mass spectrometry analyses of EFs from mice with physiological perturbations, like exercise or cold exposure, allowed the quantification of many potentially novel myokines and adipokines. Using this approach, we identify prosaposin as a secreted product of muscle and fat. Prosaposin expression stimulates thermogenic gene expression and induces mitochondrial respiration in primary fat cells. These studies together illustrate the utility of EF isolation as a discovery tool for adipokines and myokines.
MeSH term(s)	Mice ; Animals ; Extracellular Fluid/metabolism ; Saposins/metabolism ; Muscles/metabolism ; Adipose Tissue/metabolism ; Adipokines
Chemical Substances	Saposins ; Adipokines
Language	English
Publishing date	2023-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2022.12.014
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Article ; Online: Irisin acts through its integrin receptor in a two-step process involving extracellular Hsp90α

Molecular Cell. 2023 June, v. 83, no. 11 p.1903-1920.e12

2023

Abstract	Exercise benefits the human body in many ways. Irisin is secreted by muscle, increased with exercise, and conveys physiological benefits, including improved cognition and resistance to neurodegeneration. Irisin acts via αV integrins; however, a mechanistic understanding of how small polypeptides like irisin can signal through integrins is poorly understood. Using mass spectrometry and cryo-EM, we demonstrate that the extracellular heat shock protein 90α (eHsp90α) is secreted by muscle with exercise and activates integrin αVβ5. This allows for high-affinity irisin binding and signaling through an Hsp90α/αV/β5 complex. By including hydrogen/deuterium exchange data, we generate and experimentally validate a 2.98 Å RMSD irisin/αVβ5 complex docking model. Irisin binds very tightly to an alternative interface on αVβ5 distinct from that used by known ligands. These data elucidate a non-canonical mechanism by which a small polypeptide hormone like irisin can function through an integrin receptor.
Keywords	cognition ; deuterium ; exercise ; heat shock proteins ; humans ; integrins ; ligands ; mass spectrometry ; models ; muscles ; neurodegenerative diseases ; peptide hormones ; polypeptides ; irisin ; integrin ; extracellular Hsp90 ; integrin activation ; fibronectin III domain ; ligand binding ; RGD motif ; HDX-MS ; protein-protein docking
Language	English
Dates of publication	2023-06
Size	p. 1903-1920.e12.
Publishing place	Elsevier Inc.
Document type	Article ; Online
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2023.05.008
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Article ; Online: Subfornical organ insulin receptors tonically modulate cardiovascular and metabolic function.

Jeong, Jin Kwon / Horwath, Julie A / Simonyan, Hayk / Blackmore, Katherine A / Butler, Scott D / Young, Colin N

Physiological genomics

2019 Volume 51, Issue 8, Page(s) 333–341

Abstract: Insulin acts within the central nervous system through the insulin receptor to influence both metabolic and cardiovascular physiology. While a major focus has been placed on hypothalamic regions, participation of extrahypothalamic insulin receptors in ... ...

Abstract	Insulin acts within the central nervous system through the insulin receptor to influence both metabolic and cardiovascular physiology. While a major focus has been placed on hypothalamic regions, participation of extrahypothalamic insulin receptors in cardiometabolic regulation remains largely unknown. We hypothesized that insulin receptors in the subfornical organ (SFO), a forebrain circumventricular region devoid of a blood-brain barrier, are involved in metabolic and cardiovascular regulation. Immunohistochemistry in mice revealed widespread insulin receptor-positive cells throughout the rostral to caudal extent of the SFO. SFO-targeted adenoviral delivery of Cre-recombinase in insulin receptor
MeSH term(s)	Adiposity/genetics ; Animals ; Blood Pressure/genetics ; Cardiovascular System/metabolism ; Fatty Liver/genetics ; Gene Deletion ; Gene Knockdown Techniques ; Hypertriglyceridemia/genetics ; Integrases/metabolism ; Male ; Metabolic Syndrome/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Proto-Oncogene Proteins c-fos/metabolism ; Receptor, Insulin/genetics ; Receptor, Insulin/metabolism ; Subfornical Organ/metabolism ; Weight Gain/genetics
Chemical Substances	Proto-Oncogene Proteins c-fos ; Receptor, Insulin (EC 2.7.10.1) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2019-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2038823-8
ISSN	1531-2267 ; 1094-8341
ISSN (online)	1531-2267
ISSN	1094-8341
DOI	10.1152/physiolgenomics.00021.2019
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