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Masashi Kuroda

Researcher at University of Tokushima

Publications -  24
Citations -  334

Masashi Kuroda is an academic researcher from University of Tokushima. The author has contributed to research in topics: Adipose tissue & Internal medicine. The author has an hindex of 6, co-authored 19 publications receiving 117 citations. Previous affiliations of Masashi Kuroda include Japan Society for the Promotion of Science.

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Adipocyte Death and Chronic Inflammation in Obesity.

TL;DR: Accumulating evidence suggests that adipocyte death is involved in immune cell function and initiates inflammation through an interaction with macrophages; however, the precise mechanisms remain largely unknown.
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Brown-fat-mediated tumour suppression by cold-altered global metabolism

TL;DR: In this article , cold exposure of tumour-bearing mice to cold conditions markedly inhibits the growth of various types of solid tumours, including clinically untreatable cancers such as pancreatic cancers.
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Brown-fat-mediated tumour suppression by cold-altered global metabolism

TL;DR: In this paper , cold exposure of tumour-bearing mice to cold conditions markedly inhibits the growth of various types of solid tumours, including clinically untreatable cancers such as pancreatic cancers.
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UCP1-dependent and UCP1-independent metabolic changes induced by acute cold exposure in brown adipose tissue of mice.

TL;DR: Analysis of BAT after 4-h exposure to cold temperature revealed that cold exposure induces UCP1-mediated thermogenesis-dependent glucose utilization and UCP2-independent active lipid metabolism in BAT, and cold exposure largely affects amino acid metabolism inBAT.
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The PDK1-FoxO1 signaling in adipocytes controls systemic insulin sensitivity through the 5-lipoxygenase-leukotriene B4 axis.

TL;DR: It is shown that adipocyte-specific PDK1 (3′-phosphoinositide–dependent kinase 1)-deficient (A-PDK1KO) mice manifest impaired metabolic actions of insulin in adipose tissue and reduction of adipOSE tissue mass and that insulin signaling in adipocytes negatively regulates the production of LTB4 via the PDK 1−FoxO1 pathway and thereby maintains systemic insulin sensitivity.