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. 2015 Sep 23;10(9):e0135781.
doi: 10.1371/journal.pone.0135781. eCollection 2015.

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

Mohammed Seed Ahmed  1 , Julien Pelletier  2 , Hannes Leumann  2 , Harvest F Gu  2 , Claes-Göran Östenson  2
Affiliations

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

Mohammed Seed Ahmed et al. PLoS One. .

Erratum in

Abstract

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.

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Conflict of interest statement

Competing Interests: The study has received grants from the Swedish Research Council (to CGÖ); www.vr.se, The Swedish Diabetes Association, i.e. the Diabetes Fund (to CGÖ); www.sdf.se, and the Karolinska Institutet Fund (to HFG, and to CGÖ); www.ki.se. This does not alter the authors' adherence to PLOS ONE policies on sharing data and materials.

Figures

Fig 1
Fig 1. Characteristics of diabetic GK and control Wistar rats.
Before and after the 14-day treatment period, the body weights (A) and plasma glucose levels (B) were assessed in Wistar, insulin-treated GK, and non-treated GK rats. After the 14-day treatment period, the serum insulin levels (C) were assessed in the three groups of rats. Data are means ± SE (n = 10). *p < 0.05, **p < 0.01, ***p < 0.001 vs. Wistar rats; #p < 0.05, ##p < 0.01, ###p < 0.001 vs. GK rats. §§p < 0.01, §§§p < 0.001.
Fig 2
Fig 2. mRNA expressions of PKC isoforms in pancreatic islets.
mRNA expression levels of PKCα (A), PKCδ (B), PKCε (C), and PKCζ (D) in pancreatic islets of Wistar, insulin-treated GK, and non-treated GK rats are shown. Data are means ± SE (n = 10) for all PKC isoforms, except for PKCε, for which data have been shown as geometric means (95% Cl) (n = 10). *p < 0.05, **p < 0.01 vs. Wistar rats; #p < 0.05 vs. GK rats.
Fig 3
Fig 3. Protein expressions of PKC isoforms in pancreatic islets.
Representative immunoblots and densitometric analyses of PKCα (A), PKCδ (B), PKCε (C), PKCζ (D), p-PKCα (E), p-PKCε (G), and p-PKCζ (H) protein expressions in pancreatic islets of Wistar, insulin-treated GK, and non-treated GK rats are presented. The relative expression of p-PKCδ (F) was too low for densitometric analysis, thus p-PKCδ expression is shown with three different representative Western blots. Calculation of the ratio of phosphorylated protein to total protein allowed for assessing the sensitivity of proteins in pancreatic islets from the three groups of rats (I-K). Data means ± SE (n = 4). *p < 0.05, **p < 0.01 vs. Wistar rats; #p < 0.05, ##p < 0.01, ###p < 0.001 vs. GK rats.
Fig 4
Fig 4. mRNA expressions of PKC isoforms in liver.
mRNA expression levels of PKCα (A), PKCδ (B), PKCε (C), and PKCζ (D) in livers of Wistar, insulin-treated GK, and non-treated GK rats are shown. Data are means ± SE (n = 10). *p < 0.05, **p < 0.01, ***p < 0.001 vs. Wistar rats; ##p < 0.01 vs. GK rats.
Fig 5
Fig 5. Protein expressions of PKC isoforms in liver.
Representative immunoblots and densitometric analyses of PKCα (A), PKCδ (B), PKCε (C), PKCζ (D), p-PKCα (E), p-PKCδ (F), p-PKCε (G), and p-PKCζ (H) protein expressions in livers of Wistar, insulin-treated GK, and non-treated GK rats. Calculation of the ratio of phosphorylated protein to total protein allowed for assessing the sensitivity of proteins in livers from the three groups of rats (I-L). Data are means ± SE (n = 6). *p < 0.05 vs. Wistar rats.
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