open access

Vol 78, No 2 (2019)
Original article
Submitted: 2018-07-27
Accepted: 2018-09-11
Published online: 2018-10-09
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The effects of leptin on F-actin remodelling in type 1 diabetes

C. Guven1, E. Taskin1, H. Akcakaya2, R. Nurten2
·
Pubmed: 30311938
·
Folia Morphol 2019;78(2):314-324.
Affiliations
  1. Nigde Omer Halisdemir University, Turkey
  2. Istanbul University, Turkey

open access

Vol 78, No 2 (2019)
ORIGINAL ARTICLES
Submitted: 2018-07-27
Accepted: 2018-09-11
Published online: 2018-10-09

Abstract

Background: The aim of the current study is to investigate the effect of leptin on cytoskeleton structures in both in vivo and in vitro model of diabetes.

Materials and methods: For in vivo studies, leptin in different doses (240, and 480 mg/kg) was injected to the diabetic rats after 1-week of streptozotocin (STZ, 55 mg/kg) treatment. Leptin levels were analysed in serum, liver, and pancreas samples. Hepatic and pancreatic F- and G-actin expressions were determined by Western blotting. For in vitro studies, hepatic and pancreatic primary cell lines were obtained from the control rats. To these cultures, STZ (15 and 30 mM), leptin (50, 60 and 100 ng/mL), and their combinations were applied for 1, 3, and 4 weeks. After the treatment period, F-actin was visualised by the Alexa-fluor fluorescent dye. 

Results: Streptozotocin decreased the G-actin in both tissues in vivo. However, leptin caused a dose-dependent increase in G-actin levels while F-actin decreased in both tissues. Moreover, leptin caused the perimembranous condensation of actin filaments and amelioration of F-actin structures in vivo. A dose-dependent corruption of F-actin filament structures was observed in leptin-treated primary cells in vitro, while STZ also caused corruption of these filaments. Co-exposure of STZ and leptin caused the amelioration of F-actin filaments, while the peri- membranous condensation was also observed as was in vivo study. 

Conclusions: Leptin therapy could be a candidate for diabetes, but it should not be ruled out as being important the severity of diabetes and leptin doses. 

Abstract

Background: The aim of the current study is to investigate the effect of leptin on cytoskeleton structures in both in vivo and in vitro model of diabetes.

Materials and methods: For in vivo studies, leptin in different doses (240, and 480 mg/kg) was injected to the diabetic rats after 1-week of streptozotocin (STZ, 55 mg/kg) treatment. Leptin levels were analysed in serum, liver, and pancreas samples. Hepatic and pancreatic F- and G-actin expressions were determined by Western blotting. For in vitro studies, hepatic and pancreatic primary cell lines were obtained from the control rats. To these cultures, STZ (15 and 30 mM), leptin (50, 60 and 100 ng/mL), and their combinations were applied for 1, 3, and 4 weeks. After the treatment period, F-actin was visualised by the Alexa-fluor fluorescent dye. 

Results: Streptozotocin decreased the G-actin in both tissues in vivo. However, leptin caused a dose-dependent increase in G-actin levels while F-actin decreased in both tissues. Moreover, leptin caused the perimembranous condensation of actin filaments and amelioration of F-actin structures in vivo. A dose-dependent corruption of F-actin filament structures was observed in leptin-treated primary cells in vitro, while STZ also caused corruption of these filaments. Co-exposure of STZ and leptin caused the amelioration of F-actin filaments, while the peri- membranous condensation was also observed as was in vivo study. 

Conclusions: Leptin therapy could be a candidate for diabetes, but it should not be ruled out as being important the severity of diabetes and leptin doses. 

Get Citation

Keywords

cytoskeleton; diabetes; F-actin; G-actin; hepatic cells; pancreatic β-cells; leptin therapy

About this article
Title

The effects of leptin on F-actin remodelling in type 1 diabetes

Journal

Folia Morphologica

Issue

Vol 78, No 2 (2019)

Article type

Original article

Pages

314-324

Published online

2018-10-09

Page views

2330

Article views/downloads

1289

DOI

10.5603/FM.a2018.0093

Pubmed

30311938

Bibliographic record

Folia Morphol 2019;78(2):314-324.

Keywords

cytoskeleton
diabetes
F-actin
G-actin
hepatic cells
pancreatic β-cells
leptin therapy

Authors

C. Guven
E. Taskin
H. Akcakaya
R. Nurten

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