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Article ; Online: Vasoactive intestinal peptide blockade suppresses tumor growth by regulating macrophage polarization and function in CT26 tumor-bearing mice.

Kittikulsuth, Wararat / Nakano, Daisuke / Kitada, Kento / Uyama, Toru / Ueda, Natsuo / Asano, Eisuke / Okano, Keiichi / Matsuda, Yoko / Nishiyama, Akira

Scientific reports

2023 Volume 13, Issue 1, Page(s) 927

Abstract: Macrophages are a major population of immune cells in solid cancers, especially colorectal cancers. Tumor-associated macrophages (TAMs) are commonly divided into M1-like (tumor suppression) and M2-like (tumor promotion) phenotypes. Vasoactive intestinal ... ...

Abstract	Macrophages are a major population of immune cells in solid cancers, especially colorectal cancers. Tumor-associated macrophages (TAMs) are commonly divided into M1-like (tumor suppression) and M2-like (tumor promotion) phenotypes. Vasoactive intestinal peptide (VIP) is an immunoregulatory neuropeptide with a potent anti-inflammatory function. Inhibition of VIP signaling has been shown to increase CD8
MeSH term(s)	Animals ; Mice ; Colonic Neoplasms/pathology ; Macrophages/metabolism ; Mice, SCID ; Receptors, Vasoactive Intestinal Peptide/metabolism ; Receptors, Vasoactive Intestinal Peptide, Type II/metabolism ; Signal Transduction ; Vasoactive Intestinal Peptide/antagonists & inhibitors ; Vasoactive Intestinal Peptide/metabolism ; RAW 264.7 Cells
Chemical Substances	Receptors, Vasoactive Intestinal Peptide ; Receptors, Vasoactive Intestinal Peptide, Type II ; Vasoactive Intestinal Peptide (37221-79-7) ; Vipr2 protein, mouse
Language	English
Publishing date	2023-01-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-28073-6
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Article ; Online: Luseogliflozin, a SGLT2 Inhibitor, Does Not Affect Glucose Uptake Kinetics in Renal Proximal Tubules of Live Mice.

Zhang, Anqi / Nakano, Daisuke / Kittikulsuth, Wararat / Yamashita, Yuka / Nishiyama, Akira

International journal of molecular sciences

2021 Volume 22, Issue 15

Abstract: Proximal tubules (PTs) take up most of the glucose in the glomerular filtrate and return it to peritubular capillary blood. Sodium-glucose cotransporter 2 (SGLT2) at the apical membrane takes up glucose into the cell. Glucose then flows across the cells ... ...

Abstract	Proximal tubules (PTs) take up most of the glucose in the glomerular filtrate and return it to peritubular capillary blood. Sodium-glucose cotransporter 2 (SGLT2) at the apical membrane takes up glucose into the cell. Glucose then flows across the cells and is transported to the interstitium via glucose transporter 2 (GLUT2) at the basolateral membrane. However, glucose transport under SGLT2 inhibition remains poorly understood. In this study, we evaluated the dynamics of a fluorescent glucose analog, 2-NBDG, in the PTs of live mice treated with or without the SGLT2 inhibitor, luseogliflozin. We employed real-time multiphoton microscopy, in which insulin enhanced 2-NBDG uptake in skeletal muscle. Influx and efflux of 2-NBDG in PT cells were compared under hypo-, normo-, and hyperglycemic conditions. Luseogliflozin did not exert significant effects on glucose influx parameters under any level of blood glucose. Our results suggest that blood glucose level per se does not alter glucose influx or efflux kinetics in PTs. In conclusion, neither SGLT2 inhibition nor blood glucose level affect glucose uptake kinetics in PTs. The former was because of glucose influx through basolateral GLUT2, which is an established bidirectional transporter.
MeSH term(s)	Animals ; Biological Transport/drug effects ; Blood Glucose/drug effects ; Cell Line ; Glucose/metabolism ; Kidney Tubules, Proximal/drug effects ; Kidney Tubules, Proximal/metabolism ; Mice ; Mice, Inbred C57BL ; Sorbitol/analogs & derivatives ; Sorbitol/pharmacology
Chemical Substances	Blood Glucose ; Sorbitol (506T60A25R) ; 1,5-anhydro-1-(5-(4-ethoxybenzyl)-2-methoxy-4-methylphenyl)-1-thioglucitol (C596HWF74Z) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-07-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22158169
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Article ; Online: The VIPR2-selective antagonist KS-133 changes macrophage polarization and exerts potent anti-tumor effects as a single agent and in combination with an anti-PD-1 antibody.

Sakamoto, Kotaro / Kittikulsuth, Wararat / Miyako, Eijiro / Steeve, Akumwami / Ishimura, Rika / Nakagawa, Shinsaku / Ago, Yukio / Nishiyama, Akira

PloS one

2023 Volume 18, Issue 7, Page(s) e0286651

Abstract: We have previously demonstrated that KS-133 is a specific and potent antagonist of vasoactive intestinal peptide receptor 2 (VIPR2). We have also shown that vasoactive intestinal peptide-VIPR2 signaling affects the polarity and activation of tumor- ... ...

Abstract	We have previously demonstrated that KS-133 is a specific and potent antagonist of vasoactive intestinal peptide receptor 2 (VIPR2). We have also shown that vasoactive intestinal peptide-VIPR2 signaling affects the polarity and activation of tumor-associated macrophages, which is another strategy for cancer immunotherapy apart from the activation of effector T cells. In this study, we aimed to examine whether the selective blockade of VIPR2 by KS-133 changes the polarization of macrophages and induces anti-tumor effects. In the presence of KS-133, genetic markers indicative of tumor-aggressive M1-type macrophages were upregulated, and conversely, those of tumor-supportive M2-type macrophages were downregulated. Daily subcutaneous administration of KS-133 tended to suppress the growth of CT26 tumors (murine colorectal cancer-derived cells) implanted subcutaneously in Balb/c mice. To improve the pharmacological efficacy and reduce the number of doses, we examined a nanoformulation of KS-133 using the US Food and Drug Administration-approved pharmaceutical additive surfactant Cremophor® EL. KS-133 nanoparticles (NPs) were approximately 15 nm in size and stable at 4°C after preparation. Meanwhile, KS-133 was gradually released from the NPs as the temperature was increased. Subcutaneous administration of KS-133 NPs once every 3 days had stronger anti-tumor effects than daily subcutaneous administration of KS-133. Furthermore, KS-133 NPs significantly enhanced the pharmacological efficacy of an immune checkpoint-inhibiting anti-PD-1 antibody. A pharmacokinetic study suggested that the enhancement of anti-tumor activity was associated with improvement of the pharmacokinetic profile of KS-133 upon nanoformulation. Our data have revealed that specific blockade of VIPR2 by KS-133 has therapeutic potential for cancer both alone and in combination with immune checkpoint inhibitors.
MeSH term(s)	Animals ; Mice ; Cell Line, Tumor ; Immunotherapy ; Macrophages ; Neoplasms ; Receptors, Vasoactive Intestinal Peptide, Type II ; Tumor Microenvironment
Chemical Substances	Receptors, Vasoactive Intestinal Peptide, Type II ; KS-133
Language	English
Publishing date	2023-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0286651
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Article ; Online: Luseogliflozin, a SGLT2 Inhibitor, Does Not Affect Glucose Uptake Kinetics in Renal Proximal Tubules of Live Mice

Anqi Zhang / Daisuke Nakano / Wararat Kittikulsuth / Yuka Yamashita / Akira Nishiyama

International Journal of Molecular Sciences, Vol 22, Iss 8169, p

2021 Volume 8169

Abstract	Proximal tubules (PTs) take up most of the glucose in the glomerular filtrate and return it to peritubular capillary blood. Sodium-glucose cotransporter 2 (SGLT2) at the apical membrane takes up glucose into the cell. Glucose then flows across the cells and is transported to the interstitium via glucose transporter 2 (GLUT2) at the basolateral membrane. However, glucose transport under SGLT2 inhibition remains poorly understood. In this study, we evaluated the dynamics of a fluorescent glucose analog, 2-NBDG, in the PTs of live mice treated with or without the SGLT2 inhibitor, luseogliflozin. We employed real-time multiphoton microscopy, in which insulin enhanced 2-NBDG uptake in skeletal muscle. Influx and efflux of 2-NBDG in PT cells were compared under hypo-, normo-, and hyperglycemic conditions. Luseogliflozin did not exert significant effects on glucose influx parameters under any level of blood glucose. Our results suggest that blood glucose level per se does not alter glucose influx or efflux kinetics in PTs. In conclusion, neither SGLT2 inhibition nor blood glucose level affect glucose uptake kinetics in PTs. The former was because of glucose influx through basolateral GLUT2, which is an established bidirectional transporter.
Keywords	glucose handling ; proximal tubules ; intravital imaging ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	670
Language	English
Publishing date	2021-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Renal NG2-expressing cells have a macrophage-like phenotype and facilitate renal recovery after ischemic injury.

Kittikulsuth, Wararat / Nakano, Daisuke / Kitada, Kento / Suzuki, Norio / Yamamoto, Masayuki / Nishiyama, Akira

American journal of physiology. Renal physiology

2021 Volume 321, Issue 2, Page(s) F170–F178

Abstract: Pericytes play an important role in the recovery process after ischemic injury of many tissues. Brain pericytes in the peri-infarct area express macrophage markers in response to injury stimuli and are involved in neovascularization. In the kidney, nerve/ ...

Abstract	Pericytes play an important role in the recovery process after ischemic injury of many tissues. Brain pericytes in the peri-infarct area express macrophage markers in response to injury stimuli and are involved in neovascularization. In the kidney, nerve/glial antigen 2 (NG2)
MeSH term(s)	Animals ; Antigens/metabolism ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Ischemia/metabolism ; Ischemia/pathology ; Kidney/metabolism ; Kidney/pathology ; Macrophages/metabolism ; Macrophages/pathology ; Male ; Mice ; Myofibroblasts/metabolism ; Myofibroblasts/pathology ; Phagocytosis/physiology ; Phenotype ; Proteoglycans/metabolism ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology
Chemical Substances	Antigens ; Proteoglycans ; chondroitin sulfate proteoglycan 4
Language	English
Publishing date	2021-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603837-2
ISSN	1522-1466 ; 0363-6127
ISSN (online)	1522-1466
ISSN	0363-6127
DOI	10.1152/ajprenal.00011.2021
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Article ; Online: The VIPR2-selective antagonist KS-133 changes macrophage polarization and exerts potent anti-tumor effects as a single agent and in combination with an anti-PD-1 antibody.

Kotaro Sakamoto / Wararat Kittikulsuth / Eijiro Miyako / Akumwami Steeve / Rika Ishimura / Shinsaku Nakagawa / Yukio Ago / Akira Nishiyama

PLoS ONE, Vol 18, Iss 7, p e

2023 Volume 0286651

Abstract	We have previously demonstrated that KS-133 is a specific and potent antagonist of vasoactive intestinal peptide receptor 2 (VIPR2). We have also shown that vasoactive intestinal peptide-VIPR2 signaling affects the polarity and activation of tumor-associated macrophages, which is another strategy for cancer immunotherapy apart from the activation of effector T cells. In this study, we aimed to examine whether the selective blockade of VIPR2 by KS-133 changes the polarization of macrophages and induces anti-tumor effects. In the presence of KS-133, genetic markers indicative of tumor-aggressive M1-type macrophages were upregulated, and conversely, those of tumor-supportive M2-type macrophages were downregulated. Daily subcutaneous administration of KS-133 tended to suppress the growth of CT26 tumors (murine colorectal cancer-derived cells) implanted subcutaneously in Balb/c mice. To improve the pharmacological efficacy and reduce the number of doses, we examined a nanoformulation of KS-133 using the US Food and Drug Administration-approved pharmaceutical additive surfactant Cremophor® EL. KS-133 nanoparticles (NPs) were approximately 15 nm in size and stable at 4°C after preparation. Meanwhile, KS-133 was gradually released from the NPs as the temperature was increased. Subcutaneous administration of KS-133 NPs once every 3 days had stronger anti-tumor effects than daily subcutaneous administration of KS-133. Furthermore, KS-133 NPs significantly enhanced the pharmacological efficacy of an immune checkpoint-inhibiting anti-PD-1 antibody. A pharmacokinetic study suggested that the enhancement of anti-tumor activity was associated with improvement of the pharmacokinetic profile of KS-133 upon nanoformulation. Our data have revealed that specific blockade of VIPR2 by KS-133 has therapeutic potential for cancer both alone and in combination with immune checkpoint inhibitors.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Effects of molidustat, a hypoxia-inducible factor prolyl hydroxylase inhibitor, on sodium dynamics in hypertensive subtotally nephrectomized rats.

Zhang, Anqi / Nakano, Daisuke / Morisawa, Norihiko / Kitada, Kento / Kittikulsuth, Wararat / Rahman, Asadur / Morikawa, Takashi / Konishi, Yoshio / Nishiyama, Akira

Journal of pharmacological sciences

2021 Volume 146, Issue 2, Page(s) 98–104

Abstract: Hypoxia-inducible factor prolyl hydroxylase (HIF-PHD) inhibitors were developed for treatment of renal anemia. Patients applicable for HIF-PHD inhibitor treatment experience complications such as chronic kidney disease, whereby water and electrolyte ... ...

Abstract	Hypoxia-inducible factor prolyl hydroxylase (HIF-PHD) inhibitors were developed for treatment of renal anemia. Patients applicable for HIF-PHD inhibitor treatment experience complications such as chronic kidney disease, whereby water and electrolyte homeostasis is disrupted. The effects of hypoxia-inducible factor stabilization on salt accumulation in the setting of reduced renal function remain unclear. In the present study, we investigated the effect of a HIF-PHD inhibitor, molidustat, on salt distribution and excretion in rats with subtotal nephrectomy-induced chronic kidney disease. Male Wistar rats were subjected to 5/6 nephrectomy. After confirming blood pressure elevation (>150 mmHg, at 4 weeks after surgery), rats were treated with molidustat. After 1 week of treatment, molidustat did not significantly improve blood cell volume or blood pressure. Distribution of sodium, potassium, and water in skin, carcass, and bone samples was not affected by molidustat. Furthermore, molidustat had no significant effect on urinary sodium excretion or concentration in response to acute oral salt loading (1 g/kg). In conclusion, molidustat did not affect distribution or excretion of salt in rats subjected to a model of nephron loss.
MeSH term(s)	Animals ; Blood Pressure ; Disease Models, Animal ; Hypertension/metabolism ; Male ; Nephrectomy/adverse effects ; Prolyl-Hydroxylase Inhibitors/pharmacology ; Pyrazoles/pharmacology ; Rats, Wistar ; Renal Insufficiency, Chronic/etiology ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/physiopathology ; Sodium/metabolism ; Sodium/urine ; Triazoles/pharmacology ; Rats
Chemical Substances	Prolyl-Hydroxylase Inhibitors ; Pyrazoles ; Triazoles ; molidustat (9JH486CZ13) ; Sodium (9NEZ333N27)
Language	English
Publishing date	2021-03-31
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2104264-0
ISSN	1347-8648 ; 1347-8613
ISSN (online)	1347-8648
ISSN	1347-8613
DOI	10.1016/j.jphs.2021.03.007
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Article: Hepatocellular carcinoma induces body mass loss in parallel with osmolyte and water retention in rats

Kidoguchi, Satoshi / Kitada, Kento / Nakajima, Kazuki / Nakano, Daisuke / Ohsaki, Hiroyuki / Kittikulsuth, Wararat / Kobara, Hideki / Masaki, Tsutomu / Yokoo, Takashi / Takahashi, Kazuo / Titze, Jens / Nishiyama, Akira

Life sciences. 2022 Jan. 15, v. 289

2022

Abstract: The number of cancer survivors with cardiovascular disease is increasing. However, the effect of cancer on body fluid regulation remains to be clarified. In this study, we evaluated body osmolyte and water imbalance in rats with hepatocellular carcinoma ... ...

Abstract	The number of cancer survivors with cardiovascular disease is increasing. However, the effect of cancer on body fluid regulation remains to be clarified. In this study, we evaluated body osmolyte and water imbalance in rats with hepatocellular carcinoma.Wistar rats were administered diethylnitrosamine, a carcinogenic drug, to establish liver cancer. We analyzed tissue osmolyte and water content, and their associations with aldosterone secretion.Hepatocellular carcinoma rats had significantly reduced body mass and the amount of total body sodium, potassium, and water. However, these rats had significantly increased relative tissue sodium, potassium, and water content per tissue dry weight. Furthermore, these changes in sodium and water balance in hepatocellular carcinoma rats were significantly associated with increased 24-h urinary aldosterone excretion. Supplementation with 0.25% salt in drinking water improved body weight reduction associated with sodium and water retention in hepatocellular carcinoma rats, which was suppressed by treatment with spironolactone, a mineralocorticoid receptor antagonist. Additionally, the urea-driven water conservation system was activated in hepatocellular carcinoma rats.These findings suggest that hepatocellular carcinoma induces body mass loss in parallel with activation of the water conservation system including aldosterone secretion and urea accumulation to retain osmolyte and water. The osmolyte and water retention at the tissue level may be a causative factor for ascites and edema formation in liver failure rats.
Keywords	aldosterone ; antagonists ; ascites ; body fluids ; body weight ; carcinogenicity ; carcinoma ; cardiovascular diseases ; diethylnitrosamine ; drugs ; edema ; excretion ; hepatoma ; liver failure ; mineralocorticoid receptors ; potassium ; sodium ; spironolactone ; urea ; water conservation ; water content ; weight loss
Language	English
Dates of publication	2022-0115
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.120192
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Effects of post-renal anemia treatment with the HIF-PHD inhibitor molidustat on adenine-induced renal anemia and kidney disease in mice.

Li, Lei / Nakano, Daisuke / Zhang, Anqi / Kittikulsuth, Wararat / Morisawa, Norihiko / Ohsaki, Hiroyuki / Suzuki, Norio / Yamamoto, Masayuki / Nishiyama, Akira

Journal of pharmacological sciences

2020 Volume 144, Issue 4, Page(s) 229–236

Abstract: The kidneys are the major organs for erythropoietin (EPO) production in adults, and thus, kidney damage results in reduced EPO levels and anemia. Inhibitors of Hypoxia-inducible factor-prolyl hydroxylase domain-containing protein (HIF-PHD) are awaited as ...

Abstract	The kidneys are the major organs for erythropoietin (EPO) production in adults, and thus, kidney damage results in reduced EPO levels and anemia. Inhibitors of Hypoxia-inducible factor-prolyl hydroxylase domain-containing protein (HIF-PHD) are awaited as new therapeutic options for renal anemia. It can be predicted that most patients who receive HIF-PHD inhibitors have renal dysfunction as a cause of anemia. Therefore, in the present study, we investigated the effects of the HIF-PHD inhibitor molidustat on anemia and renal dysfunction when initiated after the onset of renal anemia. Male C57BL/6J mice received adenine orally to induce nephropathy. After the onset of nephropathy, the mice were treated with either vehicle or molidustat. After 4 weeks of administration, vehicle-treated mice displayed significant anemia, and molidustat ameliorated this anemia. Vehicle-treated mice exhibited reduced creatinine clearance and body weight, increased blood urea nitrogen levels, histopathological changes, immune cell infiltration, and dehydration. Molidustat reversed immune cell infiltration, dehydration, and renal fibrosis without improving renal functional parameters. In conclusion, molidustat treatment initiated after the onset of nephropathy and renal anemia reversed anemia in mice. Molidustat improved some parameters of renal abnormality, but it did not restore renal function.
MeSH term(s)	Acute Kidney Injury/chemically induced ; Acute Kidney Injury/complications ; Acute Kidney Injury/metabolism ; Adenine/adverse effects ; Anemia/drug therapy ; Anemia/etiology ; Animals ; Disease Models, Animal ; Erythropoietin/metabolism ; Hypoxia-Inducible Factor 1/antagonists & inhibitors ; Male ; Mice, Inbred C57BL ; Prolyl-Hydroxylase Inhibitors ; Pyrazoles/administration & dosage ; Pyrazoles/pharmacology ; Pyrazoles/therapeutic use ; Triazoles/administration & dosage ; Triazoles/pharmacology ; Triazoles/therapeutic use
Chemical Substances	Hypoxia-Inducible Factor 1 ; Prolyl-Hydroxylase Inhibitors ; Pyrazoles ; Triazoles ; Erythropoietin (11096-26-7) ; molidustat (9JH486CZ13) ; Adenine (JAC85A2161)
Language	English
Publishing date	2020-09-19
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2104264-0
ISSN	1347-8648 ; 1347-8613
ISSN (online)	1347-8648
ISSN	1347-8613
DOI	10.1016/j.jphs.2020.09.004
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Article ; Online: Failure to confirm a sodium-glucose cotransporter 2 inhibitor-induced hematopoietic effect in non-diabetic rats with renal anemia.

Yamazaki, Daisuke / Konishi, Yoshio / Morikawa, Takashi / Kobara, Hideki / Masaki, Tsutomu / Hitomi, Hirofumhi / Osafune, Kenji / Nakano, Daisuke / Kittikulsuth, Wararat / Nishiyama, Akira

Journal of diabetes investigation

2020 Volume 11, Issue 4, Page(s) 834–843

Abstract: Aims/introduction: Clinical studies have shown that treatment with inhibitors of sodium-glucose cotransporter 2 (SGLT2) significantly increases the hematocrit in patients with type 2 diabetes. To investigate whether SGLT2 inhibitors directly promote ... ...

Abstract	Aims/introduction: Clinical studies have shown that treatment with inhibitors of sodium-glucose cotransporter 2 (SGLT2) significantly increases the hematocrit in patients with type 2 diabetes. To investigate whether SGLT2 inhibitors directly promote erythropoietin production independently on blood glucose reduction, the hematopoietic effect of the specific SGLT2 inhibitor, luseogliflozin, was examined in non-diabetic rats with renal anemia. Materials and methods: Renal anemia was induced by treatment with adenine (200 or 600 mg/kg/day, orally for 10 days) in non-diabetic Wistar-Kyoto or Wistar rats, respectively. Luseogliflozin (10 mg/kg bodyweight) or vehicle (0.5% carboxymethyl cellulose) was then administered for 6 weeks. The hematocrit and the hemoglobin (Hb), blood urea nitrogen, plasma creatinine, and plasma erythropoietin levels were monitored. Results: Treatment with adenine decreased the hematocrit and the Hb level, which were associated with increases in the blood urea nitrogen and plasma creatinine levels. In Wistar-Kyoto rats treated with 200 mg/kg/day adenine, administration of luseogliflozin induced glycosuria, but did not change the blood urea nitrogen, plasma creatinine levels, hematocrit, Hb or plasma erythropoietin levels. Similarly, luseogliflozin treatment failed to change the hematocrit or the Hb levels in Wistar rats with renal anemia induced by 600 mg/kg/day of adenine. Plasma erythropoietin concentrations were also not different between luseogliflozin- and vehicle-treated rats. Similarly, in human erythropoietin-producing cells derived from pluripotent stem cells, luseogliflozin treatment did not change the erythropoietin level in the medium. Conclusions: These data suggest that SGLT2 inhibitor fails to exert hematopoietic effects in non-diabetic conditions.
MeSH term(s)	Adenine ; Anemia/blood ; Anemia/chemically induced ; Anemia/drug therapy ; Animals ; Disease Models, Animal ; Erythropoietin/blood ; Hematocrit ; Hematopoietic Stem Cells/drug effects ; Hemoglobins/drug effects ; Humans ; Kidney/drug effects ; Male ; Rats ; Rats, Inbred WKY ; Rats, Wistar ; Renal Insufficiency/blood ; Renal Insufficiency/chemically induced ; Renal Insufficiency/drug therapy ; Sodium-Glucose Transporter 2 Inhibitors/pharmacology ; Sorbitol/analogs & derivatives ; Sorbitol/pharmacology
Chemical Substances	Hemoglobins ; Sodium-Glucose Transporter 2 Inhibitors ; Erythropoietin (11096-26-7) ; Sorbitol (506T60A25R) ; 1,5-anhydro-1-(5-(4-ethoxybenzyl)-2-methoxy-4-methylphenyl)-1-thioglucitol (C596HWF74Z) ; Adenine (JAC85A2161)
Language	English
Publishing date	2020-02-05
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2625840-7
ISSN	2040-1124 ; 2040-1116
ISSN (online)	2040-1124
ISSN	2040-1116
DOI	10.1111/jdi.13205
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