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Article ; Online: A novel therapeutic target for kidney diseases: Lessons learned from starvation response.

Yamahara, Kosuke / Yasuda-Yamahara, Mako / Kume, Shinji

2024 Volume 254, Page(s) 108590

Abstract: The prevalence of chronic kidney disease (CKD) is increasing worldwide, making the disease an urgent clinical challenge. Caloric restriction has various anti-aging and organ-protective effects, and unraveling its molecular mechanisms may provide insight ... ...

Abstract	The prevalence of chronic kidney disease (CKD) is increasing worldwide, making the disease an urgent clinical challenge. Caloric restriction has various anti-aging and organ-protective effects, and unraveling its molecular mechanisms may provide insight into the pathophysiology of CKD. In response to changes in nutritional status, intracellular nutrient signaling pathways show adaptive changes. When nutrients are abundant, signals such as mechanistic target of rapamycin complex 1 (mTORC1) are activated, driving cell proliferation and other processes. Conversely, others, such as sirtuins and AMP-activated protein kinase, are activated during energy scarcity, in an attempt to compensate. Autophagy, a cellular self-maintenance mechanism that is regulated by such signals, has also been reported to contribute to the progression of various kidney diseases. Furthermore, in recent years, ketone bodies, which have long been considered to be detrimental, have been reported to play a role as starvation signals, and thereby to have renoprotective effects, via the inhibition of mTORC1. Therefore, in this review, we discuss the role of mTORC1, which is one of the most extensively studied nutrient-related signals associated with kidney diseases, autophagy, and ketone body metabolism; and kidney energy metabolism as a novel therapeutic target for CKD.
MeSH term(s)	Humans ; Mechanistic Target of Rapamycin Complex 1/metabolism ; Mechanistic Target of Rapamycin Complex 1/pharmacology ; Signal Transduction/physiology ; AMP-Activated Protein Kinases/metabolism ; Kidney/metabolism ; Autophagy ; Renal Insufficiency, Chronic/drug therapy
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2024-01-28
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	194735-7
ISSN	1879-016X ; 0163-7258
ISSN (online)	1879-016X
ISSN	0163-7258
DOI	10.1016/j.pharmthera.2024.108590
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Zs.A 1183: Show issues

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Article ; Online: Emerging Pathophysiological Roles of Ketone Bodies.

Tsuruta, Hiroaki / Yamahara, Kosuke / Yasuda-Yamahara, Mako / Kume, Shinji

Physiology (Bethesda, Md.)

2024 Volume 39, Issue 3

Abstract: The discovery of insulin approximately a century ago greatly improved the management of diabetes, including many of its life-threatening acute complications like ketoacidosis. This breakthrough saved many lives and extended the healthy lifespan of many ... ...

Abstract	The discovery of insulin approximately a century ago greatly improved the management of diabetes, including many of its life-threatening acute complications like ketoacidosis. This breakthrough saved many lives and extended the healthy lifespan of many patients with diabetes. However, there is still a negative perception of ketone bodies stemming from ketoacidosis. Originally, ketone bodies were thought of as a vital source of energy during fasting and exercise. Furthermore, in recent years, research on calorie restriction and its potential impact on extending healthy lifespans, as well as studies on ketone bodies, have gradually led to a reevaluation of the significance of ketone bodies in promoting longevity. Thus, in this review, we discuss the emerging and hidden roles of ketone bodies in various organs, including the heart, kidneys, skeletal muscles, and brain, as well as their potential impact on malignancies and lifespan.
MeSH term(s)	Humans ; Ketone Bodies ; Ketosis ; Diabetes Mellitus ; Longevity ; Heart
Chemical Substances	Ketone Bodies
Language	English
Publishing date	2024-01-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2158667-6
ISSN	1548-9221 ; 1548-9213
ISSN (online)	1548-9221
ISSN	1548-9213
DOI	10.1152/physiol.00031.2023
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Zs.A 2164: Show issues

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Article ; Online: Ketone Body Metabolism in Diabetic Kidney Disease.

Yamahara, Kosuke / Yasuda-Yamahara, Mako / Kuwagata, Shogo / Chin-Kanasaki, Masami / Kume, Shinji

Kidney360

2024 Volume 5, Issue 2, Page(s) 320–326

Abstract: Ketone bodies have a negative image because of ketoacidosis, one of the acute and serious complications in diabetes. The negative image persists despite the fact that ketone bodies are physiologically produced in the liver and serve as an indispensable ... ...

Abstract	Ketone bodies have a negative image because of ketoacidosis, one of the acute and serious complications in diabetes. The negative image persists despite the fact that ketone bodies are physiologically produced in the liver and serve as an indispensable energy source in extrahepatic organs, particularly during long-term fasting. However, accumulating experimental evidence suggests that ketone bodies exert various health benefits. Particularly in the field of aging research, there is growing interest in the potential organoprotective effects of ketone bodies. In addition, ketone bodies have a potential role in preventing kidney diseases, including diabetic kidney disease (DKD), a diabetic complication caused by prolonged hyperglycemia that leads to a decline in kidney function. Ketone bodies may help alleviate the renal burden from hyperglycemia by being used as an alternative energy source in patients with diabetes. Furthermore, ketone body production may reduce inflammation and delay the progression of several kidney diseases in addition to DKD. Although there is still insufficient research on the use of ketone bodies as a treatment and their effects, their renoprotective effects are being gradually proven. This review outlines the ketone body-mediated renoprotective effects in DKD and other kidney diseases.
MeSH term(s)	Humans ; Diabetic Nephropathies ; Ketone Bodies/metabolism ; Ketosis/metabolism ; Diabetes Complications ; Hyperglycemia ; Diabetes Mellitus
Chemical Substances	Ketone Bodies
Language	English
Publishing date	2024-01-16
Publishing country	United States
Document type	Review ; Journal Article
ISSN	2641-7650
ISSN (online)	2641-7650
DOI	10.34067/KID.0000000000000359
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Roles of mTOR in Diabetic Kidney Disease.

Yasuda-Yamahara, Mako / Kume, Shinji / Maegawa, Hiroshi

Antioxidants (Basel, Switzerland)

2021 Volume 10, Issue 2

Abstract: Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease and the number of patients affected is increasing worldwide. Thus, there is a need to establish a new treatment for DKD to improve the renal prognosis of diabetic patients. ... ...

Abstract	Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease and the number of patients affected is increasing worldwide. Thus, there is a need to establish a new treatment for DKD to improve the renal prognosis of diabetic patients. Recently, it has shown that intracellular metabolic abnormalities are involved in the pathogenesis of DKD. In particular, the activity of mechanistic target of rapamycin complex 1 (mTORC1), a nutrient-sensing signaling molecule, is hyperactivated in various organs of diabetic patients, which suggests the involvement of excessive mTORC1 activation in the pathogenesis of diabetes. In DKD, hyperactivated mTORC1 may be involved in the pathogenesis of podocyte damage, which causes proteinuria, and tubular cell injury that decreases renal function. Therefore, elucidating the role of mTORC1 in DKD and developing new therapeutic agents that suppress mTORC1 hyperactivity may shed new light on DKD treatments in the future.
Language	English
Publishing date	2021-02-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10020321
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Article: Roles of mTOR in Diabetic Kidney Disease

Yasuda-Yamahara, Mako / Kume, Shinji / Maegawa, Hiroshi

Antioxidants. 2021 Feb. 22, v. 10, no. 2

2021

Abstract	Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease and the number of patients affected is increasing worldwide. Thus, there is a need to establish a new treatment for DKD to improve the renal prognosis of diabetic patients. Recently, it has shown that intracellular metabolic abnormalities are involved in the pathogenesis of DKD. In particular, the activity of mechanistic target of rapamycin complex 1 (mTORC1), a nutrient-sensing signaling molecule, is hyperactivated in various organs of diabetic patients, which suggests the involvement of excessive mTORC1 activation in the pathogenesis of diabetes. In DKD, hyperactivated mTORC1 may be involved in the pathogenesis of podocyte damage, which causes proteinuria, and tubular cell injury that decreases renal function. Therefore, elucidating the role of mTORC1 in DKD and developing new therapeutic agents that suppress mTORC1 hyperactivity may shed new light on DKD treatments in the future.
Keywords	diabetes ; kidney diseases ; pathogenesis ; prognosis ; proteinuria ; rapamycin ; renal function ; therapeutics
Language	English
Dates of publication	2021-0222
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10020321
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Fructose overconsumption accelerates renal dysfunction with aberrant glomerular endothelial-mesangial cell interactions in db/db mice.

Tsuruta, Hiroaki / Yasuda-Yamahara, Mako / Yoshibayashi, Mamoru / Kuwagata, Shogo / Yamahara, Kosuke / Tanaka-Sasaki, Yuki / Chin-Kanasaki, Masami / Matsumoto, Shoma / Ema, Masatsugu / Kume, Shinji

Biochimica et biophysica acta. Molecular basis of disease

2024 Volume 1870, Issue 4, Page(s) 167074

Abstract: For the advancement of DKD treatment, identifying unrecognized residual risk factors is essential. We explored the impact of obesity diversity derived from different carbohydrate qualities, with an emphasis on the increasing trend of excessive fructose ... ...

Abstract	For the advancement of DKD treatment, identifying unrecognized residual risk factors is essential. We explored the impact of obesity diversity derived from different carbohydrate qualities, with an emphasis on the increasing trend of excessive fructose consumption and its effect on DKD progression. In this study, we utilized db/db mice to establish a novel diabetic model characterized by fructose overconsumption, aiming to uncover the underlying mechanisms of renal damage. Compared to the control diet group, the fructose-fed db/db mice exhibited more pronounced obesity yet demonstrated milder glucose intolerance. Plasma cystatin C levels were elevated in the fructose model compared to the control, and this elevation was accompanied by enhanced glomerular sclerosis, even though albuminuria levels and tubular lesions were comparable. Single-cell RNA sequencing of the whole kidney highlighted an increase in Lrg1 in glomerular endothelial cells (GECs) in the fructose model, which appeared to drive mesangial fibrosis through enhanced TGF-β1 signaling. Our findings suggest that excessive fructose intake exacerbates diabetic kidney disease progression, mediated by aberrant Lrg1-driven crosstalk between GECs and mesangial cells.
MeSH term(s)	Mice ; Animals ; Mesangial Cells ; Endothelial Cells/pathology ; Fructose/adverse effects ; Diabetic Nephropathies/pathology ; Mice, Inbred Strains ; Obesity/complications ; Cell Communication
Chemical Substances	Fructose (30237-26-4)
Language	English
Publishing date	2024-02-13
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2024.167074
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Article ; Online: Establishment of a novel mouse model of renal artery coiling-based chronic hypoperfusion-related kidney injury

Yoshimi Imamura-Uehara / Mako Yasuda-Yamahara / Shogo Kuwagata / Kosuke Yamahara / Mamoru Yoshibayashi / Yuki Tanaka-Sasaki / Akio Shimizu / Hisakazu Ogita / Masami Chin-Kanasaki / Shinji Kume

Biochemistry and Biophysics Reports, Vol 37, Iss , Pp 101607- (2024)

1481

Abstract: Renal artery stenosis-induced chronic renal ischemia is an important cause of renal dysfunction, especially in older adults, and its incidence is currently increasing. To elucidate the mechanisms underlying chronic renal hypoperfusion-induced kidney ... ...

Abstract	Renal artery stenosis-induced chronic renal ischemia is an important cause of renal dysfunction, especially in older adults, and its incidence is currently increasing. To elucidate the mechanisms underlying chronic renal hypoperfusion-induced kidney damage, we developed a novel mouse model of renal artery coiling-based chronic hypoperfusion-related kidney injury. This model exhibits decreased renal blood flow and function, atrophy, and parenchymal injury in the coiled kidney, along with compensatory hypertrophy in the non-coiled kidney, without chronic hypertension. The availability of this mouse model, which can develop renal ischemia without genetic modification, will enhance kidney disease research by serving as a new tool to investigate the effects of acquired factors (e.g., obesity and aging) and genetic factors on renal artery stenosis-related renal parenchymal damage.
Keywords	Renal hypoperfusion ; Chronic ischemia ; Artery coiling ; Animal model ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
Subject code	616
Language	English
Publishing date	2024-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Establishment of a novel mouse model of renal artery coiling-based chronic hypoperfusion-related kidney injury.

Imamura-Uehara, Yoshimi / Yasuda-Yamahara, Mako / Kuwagata, Shogo / Yamahara, Kosuke / Yoshibayashi, Mamoru / Tanaka-Sasaki, Yuki / Shimizu, Akio / Ogita, Hisakazu / Chin-Kanasaki, Masami / Kume, Shinji

Biochemistry and biophysics reports

2023 Volume 37, Page(s) 101607

Abstract	Renal artery stenosis-induced chronic renal ischemia is an important cause of renal dysfunction, especially in older adults, and its incidence is currently increasing. To elucidate the mechanisms underlying chronic renal hypoperfusion-induced kidney damage, we developed a novel mouse model of renal artery coiling-based chronic hypoperfusion-related kidney injury. This model exhibits decreased renal blood flow and function, atrophy, and parenchymal injury in the coiled kidney, along with compensatory hypertrophy in the non-coiled kidney, without chronic hypertension. The availability of this mouse model, which can develop renal ischemia without genetic modification, will enhance kidney disease research by serving as a new tool to investigate the effects of acquired factors (e.g., obesity and aging) and genetic factors on renal artery stenosis-related renal parenchymal damage.
Language	English
Publishing date	2023-12-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2831046-9
ISSN	2405-5808 ; 2405-5808
ISSN (online)	2405-5808
ISSN	2405-5808
DOI	10.1016/j.bbrep.2023.101607
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Article ; Online: Ketone bodies: A double-edged sword for mammalian life span.

Tomita, Issei / Tsuruta, Hiroaki / Yasuda-Yamahara, Mako / Yamahara, Kosuke / Kuwagata, Shogo / Tanaka-Sasaki, Yuki / Chin-Kanasaki, Masami / Fujita, Yukihiro / Nishi, Eiichiro / Katagiri, Hideki / Maegawa, Hiroshi / Kume, Shinji

Aging cell

2023 Volume 22, Issue 6, Page(s) e13833

Abstract: Accumulating evidence suggests health benefits of ketone bodies, and especially for longevity. However, the precise role of endogenous ketogenesis in mammalian life span, and the safety and efficacy of the long-term exogenous supplementation of ketone ... ...

Abstract	Accumulating evidence suggests health benefits of ketone bodies, and especially for longevity. However, the precise role of endogenous ketogenesis in mammalian life span, and the safety and efficacy of the long-term exogenous supplementation of ketone bodies remain unclear. In the present study, we show that a deficiency in endogenous ketogenesis, induced by whole-body Hmgcs2 deletion, shortens life span in mice, and that this is prevented by daily ketone body supplementation using a diet containing 1,3-butanediol, a precursor of β-hydroxybutyrate. Furthermore, feeding the 1,3-butanediol-containing diet from early in life increases midlife mortality in normal mice, but in aged mice it extends life span and prevents the high mortality associated with atherosclerosis in ApoE-deficient mice. By contrast, an ad libitum low-carbohydrate ketogenic diet markedly increases mortality. In conclusion, endogenous ketogenesis affects mammalian survival, and ketone body supplementation may represent a double-edged sword with respect to survival, depending on the method of administration and health status.
MeSH term(s)	Mice ; Animals ; Ketone Bodies ; Longevity ; Butylene Glycols ; 3-Hydroxybutyric Acid ; Mammals
Chemical Substances	Ketone Bodies ; 1,3-butylene glycol (3XUS85K0RA) ; Butylene Glycols ; 3-Hydroxybutyric Acid (TZP1275679)
Language	English
Publishing date	2023-04-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13833
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Zs.A 6581: Show issues

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Article ; Online: Limited effects of systemic or renal lipoprotein lipase deficiency on renal physiology and diseases.

Fujino, Yoshihiko / Yasuda-Yamahara, Mako / Tanaka-Sasaki, Yuki / Kuwagata, Shogo / Yamahara, Kosuke / Tagawa, Atsuko / Chin-Kanasaki, Masami / Yanagita, Motoko / Maegawa, Hiroshi / Kume, Shinji

Biochemical and biophysical research communications

2022 Volume 620, Page(s) 15–20

Abstract: Lipoprotein lipase (LPL) is an enzyme that catalyzes the hydrolysis of circulating triglyceride and the transport of fatty acids into cells. Its activity is positively regulated by insulin, and insulin resistance is associated with low LPL activity and ... ...

Abstract	Lipoprotein lipase (LPL) is an enzyme that catalyzes the hydrolysis of circulating triglyceride and the transport of fatty acids into cells. Its activity is positively regulated by insulin, and insulin resistance is associated with low LPL activity and subsequent hypertriglyceridemia. The involvement of hypertriglyceridemia in chronic kidney disease (CKD) is still under the debate in a clinical setting. Therefore, we aimed to study the role of hypertriglyceridemia in the disease using mice with systemic or renal-specific LPL deficiency. Systemic LPL deficiency was characterized by hypertriglyceridemia, but not renal injury or dyslipidemia-related conditions, such as fatty liver. Furthermore, the LPL deficiency-induced hypertriglyceridemia was not associated with a worsening of the CKD phenotype or atherosclerosis, even when CKD was induced by 5/6 nephrectomy. Next, because LPL-mediated fatty acid uptake may be important for energy metabolism in proximal tubular epithelial cells (PTECs), the role of renal LPL in renal physiology was studied by generating mice lacking LPL specifically in PTECs. These mice showed no abnormalities in their histology or renal reabsorption of micro molecules. These findings suggest that systemic and renal lipid abnormalities caused by LPL deficiency do not cause or worsen the development of renal injury, and provide novel insight regarding the potential role of lipotoxicity in the pathogenesis of obesity-related kidney injury.
MeSH term(s)	Animals ; Hyperlipoproteinemia Type I ; Hypertriglyceridemia ; Kidney/metabolism ; Lipoprotein Lipase/metabolism ; Mice ; Renal Insufficiency, Chronic/etiology ; Triglycerides/metabolism
Chemical Substances	Triglycerides ; Lipoprotein Lipase (EC 3.1.1.34)
Language	English
Publishing date	2022-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2022.06.067
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