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

• 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
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0135781

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.