Shoko Yokota

Fukushima Medical University

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Yuko Maejima

Fukushima Medical University

Kenju Shimomura

Fukushima Medical University

Shoichiro Horita

Fukushima Medical University

Tomoyuki Ono

Tohoku University

Katsuhiko Nishimori

Fukushima Medical University

Shingen Misaka

Fukushima Medical University

Shizu Hidema

Fukushima Medical University

Hiroaki Iijima

Mitsubishi Group (Japan)

Megumi Yamachi

Fukushima Medical University

Masaru Shimizu

Brigham and Women's Hospital

Cooperative Institutions

Hudson Institute

Liechtenstein Institute

John Wiley & Sons (United States)

Tohoku University

Fukushima Medical University

Mitsubishi Group (Japan)

Mitsubishi Tanabe Pharma Corporation

The University of Tokyo

Sun Yat-sen University

Kitasato University

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The undeveloped properties of GABA neurons in the ventral tegmental area promote energy intake for growth in juvenile rats

Scientific Reports (2019)

Yuko Maejima Shoko Yokota Shoichiro Horita Kenju Shimomura

Abstract Juvenile animals show higher energy intake (EI) per body weight (BW) to meet the energy requirements for growth. However, the underlying mechanisms that induce high EI/BW in juvenile animals remain unknown. The EI from a control diet (CD) and high fat diet (HFD), as well as BW changes were compared between juvenile (3 weeks old) and adult (8 weeks old) rats. BW gain and EI were increased in the HFD-fed adult rats compared to the CD-fed adult rats. However, in the juvenile rats, there were no differences in BW gain and EI between the CD-fed and HFD-fed groups. The locomotor activity was significantly increased in HFD group compared with the CD group in juvenile, but not in adult rats. Gamma-aminobutyric acid (GABA) neurons in the VTA were found to remain undeveloped with less GABAergic input into dopamine neurons in the juvenile rats. The deletion of the VTA GABA neurons in the adult rats significantly increased CD consumption, but showed almost no change in HFD consumption. These data suggest that undeveloped properties of VTA GABA neurons in juvenile rats can promote higher EI regardless of high or less palatable feeding, and contribute to growth promotion.

Gamma-Aminobutyric Acid

10.1038/s41598-019-48336-5

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Systemic Co-Administration of Low-Dose Oxytocin and Glucagon-Like Peptide 1 Additively Decreases Food Intake and Body Weight

Neuroendocrinology (2024)

Yuko Maejima Shoko Yokota Shizu Hidema Katsuhiko Nishimori Heidi de Wet

GLP-1 receptor agonists are the number one drug prescribed for the treatment of obesity and type 2 diabetes. These drugs are not, however, without side effects, and in an effort to maximize therapeutic effect while minimizing adverse effects, gut hormone co-agonists received considerable attention as new drug targets in the fight against obesity. Numerous previous reports identified the neuropeptide oxytocin (OXT) as a promising anti-obesity drug. The aims of this study were to evaluate OXT as a possible co-agonist for GLP-1 and examine the effects of its co-administration on food intake (FI) and body weight (BW) in mice.

10.1159/000538792

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Memantine has no effect on KATP channels in pancreatic β cells

BMC Research Notes (2018)

Ryota Imai Shingen Misaka Shoichiro Horita Shoko Yokota Rie Ohashi

Memantine, a drug for Alzheimer's disease, is considered to suppress excessive stimulation of N-methyl-d-aspartic acid receptors and to prevent neuronal death. However, a recent report indicated that the neuronal KATP channel also can become a target of memantine. The KATP channel is a key regulator of insulin secretion in pancreatic β cells. Therefore, if memantine could inhibit the KATP channel in pancreatic β cells, it would be an effective drug for both Alzheimer's disease and diabetes. However, there is no report on the effect of memantine on the KATP channel in pancreatic β cells. Therefore, we investigated whether memantine affect the blood glucose level, insulin secretion and KATP channel activity in pancreatic β cells. An intraperitoneal glucose tolerance test was performed with or without memantine (1 mg/kg) injection in intact mice. Insulin secretion from isolated islets was measured under low (2 mM) and high (20 mM) glucose concentrations with or without memantine (1 μM). The effect of memantine (1 μM) on KATP channel currents in isolated pancreatic β cells was recorded using the whole-cell patch-clamp technique. Memantine had no effect on the blood glucose level, insulin secretion from isolated islets or KATP channel current in pancreatic β cells.

Memantine

Pancreatic Islets

10.1186/s13104-018-3715-9

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Citations (11)

Traditional Japanese medicine Kamikihito ameliorates sucrose preference, chronic inflammation and obesity induced by a high fat diet in middle-aged mice

Frontiers in Endocrinology (2024)

Yuko Maejima Shoko Yokota Megumi Yamachi Shingen Misaka Tomoyuki Ono

The high prevalence of obesity has become a pressing global public health problem and there exists a strong association between increased BMI and mortality at a BMI of 25 kg/m 2 or higher. The prevalence of obesity is higher among middle-aged adults than among younger groups and the combination of aging and obesity exacerbate systemic inflammation. Increased inflammatory cytokines such as interleukin 6 and tumor necrosis factor alpha (TNFα) are hallmarks of obesity, and promote the secretion of hepatic C-reactive protein (CRP) which further induces systematic inflammation. The neuropeptide oxytocin has been shown to have anti-obesity and anti-inflammation effects, and also suppress sweet-tasting carbohydrate consumption in mammals. Previously, we have shown that the Japanese herbal medicine Kamikihito (KKT), which is used to treat neuropsychological stress disorders in Japan, functions as an oxytocin receptors agonist. In the present study, we further investigated the effect of KKT on body weight (BW), food intake, inflammation, and sweet preferences in middle-aged obese mice. KKT oral administration for 12 days decreased the expression of pro-inflammatory cytokines in the liver, and the plasma CRP and TNFα levels in obese mice. The effect of KKT administration was found to be different between male and female mice. In the absence of sucrose, KKT administration decreased food intake only in male mice. However, while having access to a 30% sucrose solution, both BW and food intake was decreased by KKT administration in male and female mice; but sucrose intake was decreased in female mice alone. In addition, KKT administration decreased sucrose intake in oxytocin deficient lean mice, but not in the WT lean mice. The present study demonstrates that KKT ameliorates chronic inflammation, which is strongly associated with aging and obesity, and decreases food intake in male mice as well as sucrose intake in female mice; in an oxytocin receptor dependent manner.

10.3389/fendo.2024.1387964

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Surface translocation of Kir2.1 channel induces IL-1β secretion in microglia

Molecular and Cellular Neuroscience (2022)

Yuko Maejima Shoichiro Horita Shoko Yokota Megumi Yamachi Masaru Shimizu

10.1016/j.mcn.2022.103734

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Effect of single nucleotide polymorphisms in GH gene promoter region on carcass traits and intramuscular fatty acid compositions in Japanese Black cattle

Livestock Science (2014)

Haruna Sugita Astrid Ardiyanti Shoko Yokota Shinichi Yonekura Takuji Hirayama

Intramuscular fat

Beef Cattle

Carcass weight

10.1016/j.livsci.2014.04.026

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The deletion of glucagon-like peptide-1 receptors expressing neurons in the dorsomedial hypothalamic nucleus disrupts the diurnal feeding pattern and induces hyperphagia and obesity

Nutrition & Metabolism (2021)

Yuko Maejima Shoko Yokota Masaru Shimizu Shoichiro Horita Daisuke Kobayashi

Abstract Background Feeding rhythm disruption contributes to the development of obesity. The receptors of glucagon-like peptide-1 (GLP-1) are distributed in the wide regions of the brain. Among these regions, GLP-1 receptors (GLP-1R) are expressed in the dorsomedial hypothalamic nucleus (DMH) which are known to be associated with thermogenesis and circadian rhythm development. However, the physiological roles of GLP-1R expressing neurons in the DMH remain elusive. Methods To examine the physiological role of GLP-1R expressing neurons in the DMH, saporin-conjugated exenatide4 was injected into rat brain DMH to delete GLP-1R-positive neurons. Subsequently, locomotor activity, diurnal feeding pattern, amount of food intake and body weight were measured. Results This deletion of GLP-1R-positive neurons in the DMH induced hyperphagia, the disruption of diurnal feeding pattern, and obesity. The deletion of GLP-1R expressing neurons also reduced glutamic acid decarboxylase 67 and cholecystokinin A receptor mRNA levels in the DMH. Also, it reduced the c-fos expression after refeeding in the suprachiasmatic nucleus (SCN). Thirty percent of DMH neurons projecting to the SCN expressed GLP-1R. Functionally, refeeding after fasting induced c-fos expression in the SCN projecting neurons in the DMH. As for the projection to the DMH, neurons in the nucleus tractus solitarius (NTS) were found to be projecting to the DMH, with 33% of those neurons being GLP-1-positive. Refeeding induced c-fos expression in the DMH projecting neurons in the NTS. Conclusion These findings suggest that GLP-1R expressing neurons in the DMH may mediate feeding termination. In addition, this meal signal may be transmitted to SCN neurons and change the neural activities.

10.1186/s12986-021-00582-z

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Citations (11)

Excitability of oxytocin neurons in paraventricular nucleus is regulated by voltage-gated potassium channels Kv4.2 and Kv4.3

Bioscience Biotechnology and Biochemistry (2018)

Ryota Imai Shoko Yokota Shoichiro Horita Yoichi Ueta Yuko Maejima

Oxytocin is produced by neurons in the paraventricular nucleus (PVN) and the supraoptic nucleus in the hypothalamus. Various ion channels are considered to regulate the excitability of oxytocin neurons and its secretion. A-type currents of voltage-gated potassium channels (Kv channels), generated by Kv4.2/4.3 channels, are known to be involved in the regulation of neuron excitability. However, it is unclear whether the Kv4.2/4.3 channels participate in the regulation of excitability in PVN oxytocin neurons. Here, we investigated the contribution of the Kv4.2/4.3 channels to PVN oxytocin neuron excitability. By using transgenic rat brain slices with the oxytocin-monomeric red fluorescent protein 1 fusion transgene, we examined the excitability of oxytocin neurons by electrophysiological technique. In some oxytocin neurons, the application of Kv4.2/4.3 channel blocker increased firing frequency and membrane potential with extended action potential half-width. Our present study indicates the contribution of Kv4.2/4.3 channels to PVN oxytocin neuron excitability regulation. Abbreviation: PVN, paraventricular nucleus; Oxt-mRFP1, Oxt-monometric red fluorescent protein 1; PaTx-1, Phrixotoxin-1; TEA, Tetraethylammonium Chloride; TTX, tetrodotoxin; aCSF, artificial cerebrospinal fluid;PBS, phosphate buffered saline 3v, third ventricle.

Supraoptic nucleus

Oxytocin receptor

Tetrodotoxin

10.1080/09168451.2018.1537773

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Effects of Baseline Blood Pressure and Low-Density Lipoprotein Cholesterol on Safety and Efficacy of Canagliflozin in Japanese Patients with Type 2 Diabetes Mellitus

Advances in Therapy (2015)

Nobuya Inagaki Maki Goda Shoko Yokota Nobuko Maruyama Hiroaki Iijima

Sodium glucose co-transporter 2 inhibitors decrease hemoglobin A1c (HbA1c) and blood pressure (BP) and slightly increase low-density lipoprotein cholesterol (LDL-C) in patients with type 2 diabetes mellitus (T2DM). The effects of baseline BP and LDL-C on the safety and efficacy of canagliflozin in patients were analyzed post hoc in a phase III study. Japanese patients with T2DM were classified by baseline systolic BP (SBP) of <130 or ≥130 mmHg, diastolic BP (DBP) of <80 or ≥80 mmHg, and LDL-C of <120 or ≥120 mg/dL. Canagliflozin was administered daily to patients for 52 weeks at doses of either 100 mg (n = 584) or 200 mg (n = 715). The effects of canagliflozin on the incidence of adverse events (AEs), BP, and LDL-C were evaluated. No clear differences were observed in overall safety among the subgroups classified by baseline SBP, DBP, or LDL-C, except for a slight imbalance in AEs associated with volume depletion with 200 mg of canagliflozin. The decrease in mean SBP and DBP was evident in subgroups with baseline SBP ≥130 mmHg and DBP ≥80 mmHg. Mean LDL-C was decreased in subgroups with baseline LDL-C ≥120 mg/dL at both canagliflozin doses, and they were slightly increased, but did not exceed 120 mg/dL in subgroups with baseline LDL-C <120 mg/dL. The changes in HbA1c and body weight from those observed at baseline were not different between subgroups classified by SBP, DBP, and LDL-C at either dose. The present post hoc analysis indicates that canagliflozin is well tolerated irrespective of baseline BP and LDL-C in patients with T2DM. ClinicalTrials.gov identifier, NCT01387737. Mitsubishi Tanabe Pharma Corporation.

Canagliflozin

Post-hoc analysis

Lipid Profile

10.1007/s12325-015-0255-8

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Citations (23)

General pharmacology of epinastine hydrochloride (WAL 801 CL) an antiallergic agent

Yakuri to chiryō (1992)

Noboru Ohara Makoto Takizawa Shoko Yokota Hideo Katsumura Chika Konishi

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