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Article ; Online: Central regulation of glucose metabolism in an insulin-dependent and -independent manner.

Fujikawa, Teppei

2021 Volume 33, Issue 4, Page(s) e12941

Abstract: The central nervous system (CNS) contributes significantly to glucose homeostasis. The available evidence indicates that insulin directly acts on the CNS, in particular the hypothalamus, to regulate hepatic glucose production, thereby controlling whole- ... ...

Abstract	The central nervous system (CNS) contributes significantly to glucose homeostasis. The available evidence indicates that insulin directly acts on the CNS, in particular the hypothalamus, to regulate hepatic glucose production, thereby controlling whole-body glucose metabolism. Additionally, insulin also acts on the brain to regulate food intake and fat metabolism, which may indirectly regulate glucose metabolism. Studies conducted over the last decade have found that the CNS can regulate glucose metabolism in an insulin-independent manner. Enhancement of central leptin signalling reverses hyperglycaemia in insulin-deficient rodents. Here, I review the mechanisms by which central insulin and leptin actions regulate glucose metabolism. Although clinical studies have shown that insulin treatment is currently indispensable for managing diabetes, unravelling the neuronal mechanisms underlying the central regulation of glucose metabolism will pave the way for the design of novel therapeutic drugs for diabetes.
MeSH term(s)	Animals ; Energy Metabolism/physiology ; Glucose/metabolism ; Homeostasis/physiology ; Humans ; Hypothalamus/metabolism ; Insulin/metabolism ; Leptin/metabolism ; Neurons/metabolism ; Signal Transduction/physiology
Chemical Substances	Insulin ; Leptin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-02-18
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1007517-3
ISSN	1365-2826 ; 0953-8194
ISSN (online)	1365-2826
ISSN	0953-8194
DOI	10.1111/jne.12941
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Article ; Online: Exercise-induced hypothalamic neuroplasticity: Implications for energy and glucose metabolism.

Hwang, Eunsang / Portillo, Bryan / Grose, Kyle / Fujikawa, Teppei / Williams, Kevin W

Molecular metabolism

2023 Volume 73, Page(s) 101745

Abstract: Background: Neuroplasticity refers to the brain's ability to undergo functional and structural changes in response to diverse challenges. Converging evidence supports the notion that exercise serves as a metabolic challenge, triggering the release of ... ...

Abstract	Background: Neuroplasticity refers to the brain's ability to undergo functional and structural changes in response to diverse challenges. Converging evidence supports the notion that exercise serves as a metabolic challenge, triggering the release of multiple factors both in the periphery and within the brain. These factors actively contribute to plasticity in the brain, and in turn, regulate energy and glucose metabolism. Scope of review: The primary focus of this review is to explore the impact of exercise-induced plasticity in the brain on metabolic homeostasis, with an emphasis on the role of the hypothalamus in this process. Additionally, the review provides an overview of various factors induced by exercise that contribute to energy balance and glucose metabolism. Notably, these factors exert their effects, at least in part, through actions within the hypothalamus and more broadly in the central nervous system. Major conclusions: Exercise elicits both transient and sustained changes in metabolism, accompanied by changes in neural activity within specific brain regions. Importantly, the contribution of exercise-induced plasticity and the underlying mechanisms by which neuroplasticity influences the effects of exercise are not well understood. Recent work has begun to overcome this gap in knowledge by examining the complex interactions of exercise-induced factors which alter neural circuit properties to influence metabolism.
MeSH term(s)	Hypothalamus/metabolism ; Exercise/physiology ; Brain/metabolism ; Neuronal Plasticity/physiology ; Glucose/metabolism
Chemical Substances	Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-05-31
Publishing country	Germany
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; 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.2023.101745
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Article ; Online: VMHdm/c

Yoshida, Takuya / Fujitani, Mina / Farmer, Scotlynn / Harada, Ami / Shi, Zhen / Lee, Jenny J / Tinajero, Arely / Singha, Ashish K / Fujikawa, Teppei

Molecular metabolism

2023 Volume 77, Page(s) 101792

Abstract: Objective: To adapt to metabolically challenging environments, the central nervous system (CNS) orchestrates metabolism of peripheral organs including skeletal muscle. The organ-communication between the CNS and skeletal muscle has been investigated, ... ...

Abstract	Objective: To adapt to metabolically challenging environments, the central nervous system (CNS) orchestrates metabolism of peripheral organs including skeletal muscle. The organ-communication between the CNS and skeletal muscle has been investigated, yet our understanding of the neuronal pathway from the CNS to skeletal muscle is still limited. Neurons in the dorsomedial and central parts of the ventromedial hypothalamic nucleus (VMHdm/c) expressing steroidogenic factor-1 (VMHdm/c Methods: Optogenetics was used to specifically manipulate VMHdm/c Results: Optogenetic activation of VMHdm/c Conclusions: Collectively, we propose that VMHdm/c
MeSH term(s)	Mice ; Animals ; Physical Conditioning, Animal/physiology ; Neurons/metabolism ; Signal Transduction ; Muscle, Skeletal/metabolism ; Ventromedial Hypothalamic Nucleus
Language	English
Publishing date	2023-08-24
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.2023.101792
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Article: Living without insulin: the role of leptin signaling in the hypothalamus.

Fujikawa, Teppei / Coppari, Roberto

Frontiers in neuroscience

2015 Volume 9, Page(s) 108

Abstract: Since its discovery in 1922, insulin has been thought to be required for normal metabolic homeostasis and survival. However, this view would need to be revised as recent results from different laboratories have convincingly indicated that life without ... ...

Abstract	Since its discovery in 1922, insulin has been thought to be required for normal metabolic homeostasis and survival. However, this view would need to be revised as recent results from different laboratories have convincingly indicated that life without insulin is possible in rodent models. These data indicate that particular neuronal circuitries, which include hypothalamic leptin-responsive neurons, are empowered with the capability of permitting life in complete absence of insulin. Here, we review the neuronal and peripheral mechanisms by which leptin signaling in the central nervous system (CNS) regulates glucose metabolism in an insulin-independent manner.
Language	English
Publishing date	2015-03-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2015.00108
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Article ; Online: Hypothalamic-mediated control of glucose balance in the presence and absence of insulin.

Fujikawa, Teppei / Coppari, Roberto

Aging

2014 Volume 6, Issue 2, Page(s) 92–97

Abstract: Diabetes afflicts hundreds of millions worldwide. People affected by type 1 diabetes mellitus (T1DM; the insulin-deficient form of diabetes) or type 2 diabetes mellitus (T2DM; the insulin-resistant form of diabetes) have significantly reduced life ... ...

Abstract	Diabetes afflicts hundreds of millions worldwide. People affected by type 1 diabetes mellitus (T1DM; the insulin-deficient form of diabetes) or type 2 diabetes mellitus (T2DM; the insulin-resistant form of diabetes) have significantly reduced life expectancy compared to normal individuals. This is due in part to the fact that (despite improvements) current anti-diabetic approaches are suboptimal. Indeed, severe morbidities (e.g.: cardiovascular disease, hypertension) are still too often associated with diabetes. Recent preclinical results indicate that different types of hypothalamic neurons are endowed with the ability to mediate the hyperglycemia-lowering action of the adipocyte-derived hormone leptin in an insulin-dependent and insulin-independent fashion. These results may pave the way for better anti-diabetic approaches and therefore positively impact on life expectancy of diabetic subjects.
MeSH term(s)	Aging/metabolism ; Animals ; Diabetes Mellitus/therapy ; Glucose/metabolism ; Humans ; Hypothalamus/physiology ; Insulin/physiology ; Leptin/physiology
Chemical Substances	Insulin ; Leptin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2014-03-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.100641
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Article: Tolerance to Excess-Boron Conditions Acquired by Stabilization of a BOR1 Variant with Weak Polarity in Arabidopsis.

Wakuta, Shinji / Fujikawa, Teppei / Naito, Satoshi / Takano, Junpei

Frontiers in cell and developmental biology

2016 Volume 4, Page(s) 4

Abstract: Boron (B) is a metalloid that is essential for plant growth but is toxic when present in excess. Arabidopsis BOR1 is a borate exporter, facilitating B translocation from root to shoot under limited-B conditions. BOR1 shows stele side polar localization ... ...

Abstract	Boron (B) is a metalloid that is essential for plant growth but is toxic when present in excess. Arabidopsis BOR1 is a borate exporter, facilitating B translocation from root to shoot under limited-B conditions. BOR1 shows stele side polar localization in the plasma membrane of various root cells, presumably to support B translocation toward the stele. BOR1 is degraded under high-B supply through vacuolar sorting via ubiquitination at the K590 residue to prevent the accumulation of B to a toxic level in shoots. A previous study showed that overexpression of BOR1 under control of the cauliflower mosaic virus 35S RNA promoter improved the growth of Arabidopsis under limited-B conditions without affecting the growth under sufficient-to-excess-B conditions. In this study, we unexpectedly found that ubiquitous expression of a stabilized BOR1 variant improved tolerance to excess-B in Arabidopsis. We established transgenic plants expressing BOR1-GFP fused with hygromycin phosphotransferase (HPT) and BOR1(K590A)-GFP-HPT under control of the ubiquitin 10 promoter. BOR1-GFP-HPT and BOR1(K590A)-GFP-HPT were expressed in various cell types in leaves and roots and showed weak polar localization in root tip cells. BOR1-GFP-HPT, but not BOR1(K590A)-GFP-HPT, was degraded through an endocytic pathway under high-B conditions. Transgenic plants with the stabilized variant BOR1(K590A)-GFP-HPT showed improved root and shoot growth under excess-B conditions. The concentration of B was greater in the shoots of plants with BOR1(K590A)-GFP-HPT or BOR1-GFP-HPT than in those of untransformed wild-type plants. These results suggest that BOR1(K590A)-GFP-HPT confers tolerance to excess-B by excluding B from the cytosol of shoot cells. Results from this study indicate the potential for engineering the trafficking properties of a transporter to produce plants that are tolerant to mineral stress.
Language	English
Publishing date	2016-02-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2016.00004
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Article ; Online: Glucose-Lowering by Leptin in the Absence of Insulin Does Not Fully Rely on the Central Melanocortin System in Male Mice.

Singha, Ashish K / Yamaguchi, Junya / Gonzalez, Nancy S / Ahmed, Newaz / Toney, Glenn M / Fujikawa, Teppei

Endocrinology

2019 Volume 160, Issue 3, Page(s) 651–663

Abstract: Central leptin administration can ameliorate hyperglycemia in insulin-deficient rodent models independently of insulin; however, the underlying neuronal mechanism are unclear. Here, we investigate the contribution of key elements within the central ... ...

Abstract	Central leptin administration can ameliorate hyperglycemia in insulin-deficient rodent models independently of insulin; however, the underlying neuronal mechanism are unclear. Here, we investigate the contribution of key elements within the central melanocortin system by examining whether central leptin injection can ameliorate hyperglycemia in total insulin-deficient mice that either lacked melanocortin 4 receptors (MC4Rs) in the whole body [knockout (KO); MC4R KO] or selectively, in single-minded homolog 1 (SIM1)-expressing neurons (SIM1ΔMC4R). We further investigated the contribution of leptin receptors (LEPRs) in agouti-related protein (AgRP)-expressing neurons (AgRP∆LEPR). Leptin injections into the cerebral ventricle attenuated mortality and elevated blood glucose in total insulin-deficient MC4R KO mice. Total insulin-deficient SIM1ΔMC4R mice exhibited the same magnitude reduction of blood glucose in response to leptin injections as MC4R KO mice, suggesting SIM1 neurons are key to MC4R-mediated, insulin-independent, glucose-lowering effects of leptin. Central leptin injection also partially rescued glucose levels in total insulin-deficient AgRP∆LEPR mice. In brain slice studies, basal discharge of AgRP neurons from mice with total insulin deficiency was increased and leptin partially reduced their firing rate without membrane potential hyperpolarization. Collectively, our findings indicate that, contrary to glucose-lowering effects of leptin in the presence of insulin or partial insulin deficiency, MC4Rs in SIM1 neurons and LEPRs in AgRP neurons are not solely responsible for glucose-lowering effects of leptin in total insulin deficiency. This indicates that the central melanocortin system operates with other neuronal systems to fully mediate glucose-lowering effects of leptin in an insulin-independent manner.
MeSH term(s)	Animals ; Arcuate Nucleus of Hypothalamus/metabolism ; Blood Glucose/metabolism ; Insulin/deficiency ; Leptin/physiology ; Male ; Mice ; Paraventricular Hypothalamic Nucleus/metabolism ; Receptor, Melanocortin, Type 4/metabolism ; Receptors, Leptin/metabolism
Chemical Substances	Blood Glucose ; Insulin ; Leptin ; Receptor, Melanocortin, Type 4 ; Receptors, Leptin
Language	English
Publishing date	2019-03-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2018-00907
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Article: An enteroendocrine-microbial axis in the large intestine controls host metabolism.

Tan, Shuai / Santolaya, Jacobo / Wright, Tiffany Freeney / Liu, Qi / Fujikawa, Teppei / Chi, Sensen / Bergstrom, Colin P / Lopez, Adam / Chen, Qing / do Vale, Goncalo Dias / McDonald, Jeffrey G / Jia, Da / Elmquist, Joel K / Sifuentes-Dominguez, Luis / Burstein, Ezra

Research square

2023

Abstract: Nutrient handling is an essential function of the gastrointestinal tract. Most nutrient absorption occurs in the small intestine and is coordinated by hormone-producing intestinal epithelial cells known as enteroendocrine cells (EECs) ...

Abstract	Nutrient handling is an essential function of the gastrointestinal tract. Most nutrient absorption occurs in the small intestine and is coordinated by hormone-producing intestinal epithelial cells known as enteroendocrine cells (EECs)
Language	English
Publishing date	2023-07-06
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3112286/v1
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Article: Leptin Receptors in RIP-Cre

Singha, Ashish / Palavicini, Juan Pablo / Pan, Meixia / Farmer, Scotlynn / Sandoval, Darleen / Han, Xianlin / Fujikawa, Teppei

Frontiers in endocrinology

2020 Volume 11, Page(s) 588447

Abstract: Leptin is a potent endocrine hormone produced by adipose tissue and regulates a broad range of whole-body metabolism such as glucose and lipid metabolism, even without insulin. Central leptin signaling can lower hyperglycemia in insulin-deficient rodents ...

Abstract	Leptin is a potent endocrine hormone produced by adipose tissue and regulates a broad range of whole-body metabolism such as glucose and lipid metabolism, even without insulin. Central leptin signaling can lower hyperglycemia in insulin-deficient rodents via multiple mechanisms, including improvements of dyslipidemia. However, the specific neurons that regulate anti-dyslipidemia effects of leptin remain unidentified. Here we report that leptin receptors (LEPRs) in neurons expressing Cre recombinase driven by a short fragment of a promoter region of
MeSH term(s)	Animals ; Dyslipidemias/drug therapy ; Dyslipidemias/etiology ; Dyslipidemias/metabolism ; Dyslipidemias/pathology ; Glucose/metabolism ; Hyperglycemia/drug therapy ; Hyperglycemia/etiology ; Hyperglycemia/metabolism ; Hyperglycemia/pathology ; Insulin/deficiency ; Integrases/metabolism ; Leptin/pharmacology ; Male ; Mice ; Mice, Transgenic ; Neurons/metabolism ; Receptors, Leptin/physiology
Chemical Substances	Insulin ; Leptin ; Receptors, Leptin ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2020-09-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2020.588447
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Article ; Online: Deadenylase-dependent mRNA decay of GDF15 and FGF21 orchestrates food intake and energy expenditure.

Katsumura, Sakie / Siddiqui, Nadeem / Goldsmith, Michael Rock / Cheah, Jaime H / Fujikawa, Teppei / Minegishi, Genki / Yamagata, Atsushi / Yabuki, Yukako / Kobayashi, Kaoru / Shirouzu, Mikako / Inagaki, Takeshi / Huang, Tim H-M / Musi, Nicolas / Topisirovic, Ivan / Larsson, Ola / Morita, Masahiro

Cell metabolism

2022 Volume 34, Issue 4, Page(s) 564–580.e8

Abstract: Hepatokines, secretory proteins from the liver, mediate inter-organ communication to maintain a metabolic balance between food intake and energy expenditure. However, molecular mechanisms by which hepatokine levels are rapidly adjusted following stimuli ... ...

Abstract	Hepatokines, secretory proteins from the liver, mediate inter-organ communication to maintain a metabolic balance between food intake and energy expenditure. However, molecular mechanisms by which hepatokine levels are rapidly adjusted following stimuli are largely unknown. Here, we unravel how CNOT6L deadenylase switches off hepatokine expression after responding to stimuli (e.g., exercise and food) to orchestrate energy intake and expenditure. Mechanistically, CNOT6L inhibition stabilizes hepatic Gdf15 and Fgf21 mRNAs, increasing corresponding serum protein levels. The resulting upregulation of GDF15 stimulates the hindbrain to suppress appetite, while increased FGF21 affects the liver and adipose tissues to induce energy expenditure and lipid consumption. Despite the potential of hepatokines to treat metabolic disorders, their administration therapies have been challenging. Using small-molecule screening, we identified a CNOT6L inhibitor enhancing GDF15 and FGF21 hepatokine levels, which dramatically improves diet-induced metabolic syndrome. Our discovery, therefore, lays the foundation for an unprecedented strategy to treat metabolic syndrome.
MeSH term(s)	Animals ; Eating ; Energy Metabolism/genetics ; Fibroblast Growth Factors/metabolism ; Growth Differentiation Factor 15/genetics ; Growth Differentiation Factor 15/metabolism ; Humans ; Liver/metabolism ; Metabolic Syndrome/metabolism ; Mice ; RNA Stability/genetics ; RNA Stability/physiology ; Ribonucleases/metabolism
Chemical Substances	GDF15 protein, human ; Growth Differentiation Factor 15 ; fibroblast growth factor 21 ; Fibroblast Growth Factors (62031-54-3) ; CNOT6L protein, human (EC 3.1.-) ; Cnot6l protein, mouse (EC 3.1.-) ; Ribonucleases (EC 3.1.-)
Language	English
Publishing date	2022-04-05
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.2022.03.005
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