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Role of TRPM5 channel in insulin secretion from rat β-cells.: TRPM5 and insulin secretion
KTH, School of Engineering Sciences (SCI), Applied Physics. (Hjalmar Brismar)ORCID iD: 0000-0003-0374-4411
Karolinska Institutet.
Karolinska Insititutet.
Karolinska Institutet.
2014 (English)In: Pancreas, ISSN 0885-3177, E-ISSN 1536-4828, Vol. 43, no 4, p. 597-604Article in journal, Editorial material (Refereed) Published
Abstract [en]

OBJECTIVE:

Several studies have reported that the transient receptor potential melastatin-like subtype 5 (TRPM5) channel, a Ca(2+)-activated monovalent cation channel, is involved in the stimulus-secretion coupling in the mouse pancreatic β-cells. We have studied the role of the TRPM5 channel in regulating insulin secretion and cytoplasmic free Ca(2+) concentration ([Ca(2+)](i)) in the rat β-cells by using triphenylphosphine oxide, a selective inhibitor of the channel.

METHODS:

Insulin secretion from islets from Sprague-Dawley rats was measured in batch incubations. Cytoplasmic free Ca(2+) concentration was measured from single β-cells by fura-2-based microfluorometry.

RESULTS:

Triphenylphosphine oxide did not alter insulin secretion and [Ca(2+)](i) response triggered by KCl or fructose. It inhibited insulin secretion in response to glucose, L-arginine, and glucagon-like peptide 1. It also inhibited glucose-induced insulin secretion by mechanisms that are independent of the adenosine triphosphate-sensitive potassium channels and [Ca(2+)](i) increase.

CONCLUSIONS:

Our results suggest that in the rat islets, TRPM5 is involved in mediating insulin secretion by glucose and l-arginine and in potentiating the glucose-induced insulin secretion by glucagon-like peptide 1.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2014. Vol. 43, no 4, p. 597-604
Keywords [en]
TRPM5, Islets of langerhans, calcium signaling, insulin secretion
National Category
Medical and Health Sciences
Research subject
Medical Technology
Identifiers
URN: urn:nbn:se:kth:diva-204559OAI: oai:DiVA.org:kth-204559DiVA, id: diva2:1085183
Funder
Swedish Society of Medicine
Note

QC 20170328

Available from: 2017-03-28 Created: 2017-03-28 Last updated: 2017-11-29Bibliographically approved
In thesis
1. Studies on molecular mechanisms in calcium signaling and cellular energy consumption
Open this publication in new window or tab >>Studies on molecular mechanisms in calcium signaling and cellular energy consumption
2017 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Ion signaling plays fundamental role in cell survival. Na+ and Ca2+ are critical players in ion signaling. Cells spend the major amount of energy to maintain and regulate Na+ and Ca2+ gradients across the cell membrane. Any disruption in cellular energy consumption by plasma membrane ATPases affects ion signaling and vice versa. This thesis is a combination of four separate research studies. In the first study, We measured ATP consumption dynamics of Na+/K+-ATPase using a genetically encoded fluorescent indicator called Perceval HR. we demonstrate that PercevalHR is an excellent tool to visualize ATP:ADP in mammalian cells.

In the second study, We studied the role of calcium signaling and TRP channels in angiotensin II type 1 receptor  signaling cascade. We prove that low inhibition of CaV1.2 with physiological and therapeutically relevant concentration of Angiotensin II up regulate AT1R signaling.

In the third study, We studied the role of the TRPM5 channel in regulating insulin secretion, and cytoplasmic free calcium concentration in the rat β-cells by usingtriphenyl phosphine oxide, a selective inhibitor of the channel.

In the fourth study, We tested whether, the genetically engineered human β-cell line (EndoC-BH1) could be used as models for studying Ca2+signaling in the context of Type II Diabetes. We found that the EndoC-BH1 cells could be a relevant model to study stimulus-secretion coupling and Ca2+ signaling in the human β-cells.

Place, publisher, year, edition, pages
Stockholm: KTH Royal Institute of Technology, 2017. p. 76
Keywords
ca2+ signaling, ATP, PercevalHR, NKA, diabetes, Angiotensin
National Category
Medical and Health Sciences
Research subject
Biological Physics
Identifiers
urn:nbn:se:kth:diva-204418 (URN)978-91-7729-337-8 (ISBN)
Public defence
2017-04-19, Fire, Scilifelab, Tomtebodavägen 23a, Solna, 09:00 (English)
Opponent
Supervisors
Note

QC 20170328

Available from: 2017-03-28 Created: 2017-03-27 Last updated: 2017-03-28Bibliographically approved

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