抄録
Background: Overweight and obesity are defined as excessive or abnormal fat accumulation in adipose tissues, and increase the risk of morbidity in many diseases, including hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, and stroke, through pathophysiological mechanisms. There is strong evidence that weight loss reduces the risk of metabolic syndrome by limiting blood pressure and improving the levels of serum triglycerides, total cholesterol, low-density lipoprotein-cholesterol, and high-density lipoprotein-cholesterol. To date, several attempts have been made to develop effective anti-obesity medication or weight-loss drugs; however, satisfactory drugs for clinical use have not yet been developed. Therefore, elucidation of the molecular mechanisms driving fat metabolism (adipogenesis and lipolysis) represents the first step in developing clinically useful drugs and/or therapeutic treatments to control obesity. Highlight: In our previous study on intracellular signaling of phospholipase C-related catalytically inactive protein (PRIP), we generated and analyzed Prip-double knockout (Prip-DKO) mice. Prip-DKO mice showed tolerance against insulin resistance and a lean phenotype with low fat mass. Here, we therefore reviewed the involvement of PRIP in fat metabolism and energy expenditure. We conclude that PRIP, a protein phosphatase-binding protein, can modulate fat metabolism via phosphoregulation of adipose lipolysis-related molecules, and regulates non-shivering heat generation in brown adipocytes. Conclusion: We propose PRIP as a new therapeutic target for controlling obesity or developing novel anti-obesity drugs.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 65-72 |
| ページ数 | 8 |
| ジャーナル | journal of oral biosciences |
| 巻 | 61 |
| 発行部数 | 2 |
| DOI | |
| 出版物ステータス | 出版済み - 6 1 2019 |
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All Science Journal Classification (ASJC) codes
- Medicine (miscellaneous)
- Dentistry(all)
- Biochemistry, Genetics and Molecular Biology(all)
これを引用
Phospholipase C-related catalytically inactive protein : A novel signaling molecule for modulating fat metabolism and energy expenditure. / Kanematsu, Takashi; Oue, Kana; Okumura, Toshiya; Harada, Kae; Yamawaki, Yosuke; Asano, Satoshi; Mizokami, Akiko; Irifune, Masahiro; Hirata, Masato.
：: journal of oral biosciences, 巻 61, 番号 2, 01.06.2019, p. 65-72.研究成果: ジャーナルへの寄稿 › 評論記事
}
TY - JOUR
T1 - Phospholipase C-related catalytically inactive protein
T2 - A novel signaling molecule for modulating fat metabolism and energy expenditure
AU - Kanematsu, Takashi
AU - Oue, Kana
AU - Okumura, Toshiya
AU - Harada, Kae
AU - Yamawaki, Yosuke
AU - Asano, Satoshi
AU - Mizokami, Akiko
AU - Irifune, Masahiro
AU - Hirata, Masato
PY - 2019/6/1
Y1 - 2019/6/1
N2 - Background: Overweight and obesity are defined as excessive or abnormal fat accumulation in adipose tissues, and increase the risk of morbidity in many diseases, including hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, and stroke, through pathophysiological mechanisms. There is strong evidence that weight loss reduces the risk of metabolic syndrome by limiting blood pressure and improving the levels of serum triglycerides, total cholesterol, low-density lipoprotein-cholesterol, and high-density lipoprotein-cholesterol. To date, several attempts have been made to develop effective anti-obesity medication or weight-loss drugs; however, satisfactory drugs for clinical use have not yet been developed. Therefore, elucidation of the molecular mechanisms driving fat metabolism (adipogenesis and lipolysis) represents the first step in developing clinically useful drugs and/or therapeutic treatments to control obesity. Highlight: In our previous study on intracellular signaling of phospholipase C-related catalytically inactive protein (PRIP), we generated and analyzed Prip-double knockout (Prip-DKO) mice. Prip-DKO mice showed tolerance against insulin resistance and a lean phenotype with low fat mass. Here, we therefore reviewed the involvement of PRIP in fat metabolism and energy expenditure. We conclude that PRIP, a protein phosphatase-binding protein, can modulate fat metabolism via phosphoregulation of adipose lipolysis-related molecules, and regulates non-shivering heat generation in brown adipocytes. Conclusion: We propose PRIP as a new therapeutic target for controlling obesity or developing novel anti-obesity drugs.
AB - Background: Overweight and obesity are defined as excessive or abnormal fat accumulation in adipose tissues, and increase the risk of morbidity in many diseases, including hypertension, dyslipidemia, type 2 diabetes, coronary heart disease, and stroke, through pathophysiological mechanisms. There is strong evidence that weight loss reduces the risk of metabolic syndrome by limiting blood pressure and improving the levels of serum triglycerides, total cholesterol, low-density lipoprotein-cholesterol, and high-density lipoprotein-cholesterol. To date, several attempts have been made to develop effective anti-obesity medication or weight-loss drugs; however, satisfactory drugs for clinical use have not yet been developed. Therefore, elucidation of the molecular mechanisms driving fat metabolism (adipogenesis and lipolysis) represents the first step in developing clinically useful drugs and/or therapeutic treatments to control obesity. Highlight: In our previous study on intracellular signaling of phospholipase C-related catalytically inactive protein (PRIP), we generated and analyzed Prip-double knockout (Prip-DKO) mice. Prip-DKO mice showed tolerance against insulin resistance and a lean phenotype with low fat mass. Here, we therefore reviewed the involvement of PRIP in fat metabolism and energy expenditure. We conclude that PRIP, a protein phosphatase-binding protein, can modulate fat metabolism via phosphoregulation of adipose lipolysis-related molecules, and regulates non-shivering heat generation in brown adipocytes. Conclusion: We propose PRIP as a new therapeutic target for controlling obesity or developing novel anti-obesity drugs.
UR - http://www.scopus.com/inward/record.url?scp=85065984451&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85065984451&partnerID=8YFLogxK
U2 - 10.1016/j.job.2019.04.002
DO - 10.1016/j.job.2019.04.002
M3 - Review article
C2 - 31109860
AN - SCOPUS:85065984451
VL - 61
SP - 65
EP - 72
JO - Journal of Oral Biosciences
JF - Journal of Oral Biosciences
SN - 1349-0079
IS - 2
ER -