Expression of Protein Kinase C Isoforms in Pancreatic Islets and Liver of Male Goto-Kakizaki Rats, a Model of Type 2 Diabetes

Protein kinase C (PKC) is a family of protein kinases controlling protein phosphorylation and playing important roles in the regulation of metabolism. We have investigated expression levels of PKC isoforms in pancreatic islets and liver of diabetic Goto-Kakizaki (GK) rats with and without insulin tr...

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Published in:PloS one 2015-09, Vol.10 (9), p.e0135781-e0135781
Main Authors: Seed Ahmed, Mohammed, Ahmed, Mohammed Seed, Pelletier, Julien, Leumann, Hannes, Gu, Harvest F, Östenson, Claes-Göran
Format: Article
Language:English
Subjects:
Animals
Blood Glucose
Cell growth
Development and progression
Diabetes mellitus
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - metabolism
Disease Models, Animal
Gene Expression
Genetic aspects
Glucose
Glucose - metabolism
Homeostasis
Hyperglycemia
Insulin
Insulin - metabolism
Insulin resistance
Islets of Langerhans
Islets of Langerhans - metabolism
Isoenzymes
Isoforms
Kinases
Life assessment
Liver
Liver - metabolism
Male
Medicin och hälsovetenskap
Metabolism
Oncorhynchus mykiss
Pancreas
Phosphorylation
Physiological aspects
Protein kinase C
Protein Kinase C - genetics
Protein Kinase C - metabolism
Protein kinases
Rats
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rodents
Type 2 diabetes
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container_issue 9
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creator Seed Ahmed, Mohammed
Ahmed, Mohammed Seed
Pelletier, Julien
Leumann, Hannes
Gu, Harvest F
Östenson, Claes-Göran
description Protein kinase C (PKC) is a family of protein kinases controlling protein phosphorylation and playing important roles in the regulation of metabolism. We have investigated expression levels of PKC isoforms in pancreatic islets and liver of diabetic Goto-Kakizaki (GK) rats with and without insulin treatment to evaluate their association with glucose homeostasis. mRNA and protein expression levels of PKC isoforms were assessed in pancreatic islets and liver of Wistar rats and GK rats with or without insulin treatment. PKCα and PKCζ mRNA expressions were down-regulated in islets of GK compared with Wistar rats. PKCα and phosphorylated PKCα (p-PKCα) protein expressions were decreased in islets of GK compared with insulin-treated GK and Wistar rats. PKCζ protein expression in islets was reduced in GK and insulin-treated GK compared with Wistar rats, but p-PKCζ was decreased only in GK rats. Islet PKCε mRNA and protein expressions were lower in GK compared with insulin-treated GK and Wistar rats. In liver, PKCδ and PKCζ mRNA expressions were decreased in both GK and insulin-treated GK compared with Wistar rats. Hepatic PKCζ protein expression was diminished in both GK rats with and without insulin treatment compared with Wistar rats. Hepatic PKCε mRNA expression was down-regulated in insulin-treated GK compared with GK and Wistar rats. PKCα, PKCε, and p-PKCζ expressions were secondary to hyperglycaemia in GK rat islets. Hepatic PKCδ and PKCζ mRNA expressions were primarily linked to hyperglycaemia. Additionally, hepatic PKCε mRNA expression could be under control of insulin.
doi_str_mv 10.1371/journal.pone.0135781
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We have investigated expression levels of PKC isoforms in pancreatic islets and liver of diabetic Goto-Kakizaki (GK) rats with and without insulin treatment to evaluate their association with glucose homeostasis. mRNA and protein expression levels of PKC isoforms were assessed in pancreatic islets and liver of Wistar rats and GK rats with or without insulin treatment. PKCα and PKCζ mRNA expressions were down-regulated in islets of GK compared with Wistar rats. PKCα and phosphorylated PKCα (p-PKCα) protein expressions were decreased in islets of GK compared with insulin-treated GK and Wistar rats. PKCζ protein expression in islets was reduced in GK and insulin-treated GK compared with Wistar rats, but p-PKCζ was decreased only in GK rats. Islet PKCε mRNA and protein expressions were lower in GK compared with insulin-treated GK and Wistar rats. In liver, PKCδ and PKCζ mRNA expressions were decreased in both GK and insulin-treated GK compared with Wistar rats. Hepatic PKCζ protein expression was diminished in both GK rats with and without insulin treatment compared with Wistar rats. Hepatic PKCε mRNA expression was down-regulated in insulin-treated GK compared with GK and Wistar rats. PKCα, PKCε, and p-PKCζ expressions were secondary to hyperglycaemia in GK rat islets. Hepatic PKCδ and PKCζ mRNA expressions were primarily linked to hyperglycaemia. Additionally, hepatic PKCε mRNA expression could be under control of insulin.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26398746</pmid><doi>10.1371/journal.pone.0135781</doi><oa>free_for_read</oa></addata></record>
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1932-6203
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subjects Animals
Blood Glucose
Cell growth
Development and progression
Diabetes mellitus
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - genetics
Diabetes Mellitus, Type 2 - metabolism
Disease Models, Animal
Gene Expression
Genetic aspects
Glucose
Glucose - metabolism
Homeostasis
Hyperglycemia
Insulin
Insulin - metabolism
Insulin resistance
Islets of Langerhans
Islets of Langerhans - metabolism
Isoenzymes
Isoforms
Kinases
Life assessment
Liver
Liver - metabolism
Male
Medicin och hälsovetenskap
Metabolism
Oncorhynchus mykiss
Pancreas
Phosphorylation
Physiological aspects
Protein kinase C
Protein Kinase C - genetics
Protein Kinase C - metabolism
Protein kinases
Rats
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rodents
Type 2 diabetes
title Expression of Protein Kinase C Isoforms in Pancreatic Islets and Liver of Male Goto-Kakizaki Rats, a Model of Type 2 Diabetes
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