• Korean Journal of Veterinary Research
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• v.39 no.4
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• pp.673-678
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• 1999

The distribution and relative frequency of insulin-immunoreactive cells in the pancreas was studied during developmental stages (fetus, neonate, 1-month-old, 6-month-old and adult) of the Korean native goat by immunohistochemical methods. The different distribution and relative frequency of glucagon-immunoreactive cells in the pancreas of the Korean native goat was observed during development. Insulin-immunoreactive cells were detected in the exocrine and endocrine portions (pancreatic islets) of the all ages, and in the duct of the 6-month-old. The relative frequencies of these cells were increased in the pancreatic islets with ages but decreased in the exocrine portions. Generally, they were distributed in the interacinar spaces or central zone of the pancreatic islets in all ages. However, the distributions and relative frequencies in the pancreatic islets of the neonate Korean native goat were divided into three patterns : 1) located in the inner zone with numerous frequencies, 2) the peripheral zone of the pancreatic islet with moderate frequencies and 3) the peripheral zone of the pancreatic islet with a few frequencies patterns.

• BMB Reports
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• v.56 no.7
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• pp.385-391
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• 2023

Aspartate-glutamate carrier 2 (AGC2, citrin) is a mitochondrial carrier expressed in the liver that transports aspartate from mitochondria into the cytosol in exchange for glutamate. The AGC2 is the main component of the malate-aspartate shuttle (MAS) that ensures indirect transport of NADH produced in the cytosol during glycolysis, lactate oxidation to pyruvate, and ethanol oxidation to acetaldehyde into mitochondria. Through MAS, AGC2 is necessary to maintain intracellular redox balance, mitochondrial respiration, and ATP synthesis. Through elevated cytosolic Ca²⁺ level, the AGC2 is stimulated by catecholamines and glucagon during starvation, exercise, and muscle wasting disorders. In these conditions, AGC2 increases aspartate input to the urea cycle, where aspartate is a source of one of two nitrogen atoms in the urea molecule (the other is ammonia), and a substrate for the synthesis of fumarate that is gradually converted to oxaloacetate, the starting substrate for gluconeogenesis. Furthermore, aspartate is a substrate for the synthesis of asparagine, nucleotides, and proteins. It is concluded that AGC2 plays a fundamental role in the compartmentalization of aspartate and glutamate metabolism and linkage of the reactions of MAS, glycolysis, gluconeogenesis, amino acid catabolism, urea cycle, protein synthesis, and cell proliferation. Targeting of AGC genes may represent a new therapeutic strategy to fight cancer.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.201-209
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• 2018

G protein-coupled receptor 119 (GPR119) is expressed in the pancreas and gastrointestinal tract, and its activation promotes insulin secretion in the beta cells of the pancreatic islets as well as the secretion of glucagon-like peptide-1 (GLP-1) in intestinal L cells, consequently improving glucose-stimulated insulin secretion. Due to this dual mechanism of action, the development of small-molecule GPR119 agonists has received significant interest for the treatment of type 2 diabetes. We newly synthesized 1,2,4-triazolone derivatives of GPR119 agonists, which demonstrated excellent outcomes in a cyclic adenosine monophosphate (cAMP) assay. Among the synthesized derivatives, YH18968 showed cAMP=2.8 nM; in GLUTag cell, GLP-1secretion=2.3 fold; in the HIT-T15 cell, and insulin secretion=1.9 fold. Single oral administration of YH18968 improved glucose tolerance and combined treatment with a dipeptidyl peptidase 4 (DPP-4) inhibitor augmented the glucose lowering effect as well as the plasma level of active GLP-1 in normal mice. Single oral administration of YH18968 improved glucose tolerance in a diet induced obese mice model. This effect was maintained after repeated dosing for 4 weeks. The results indicate that YH18968 combined with a DPP-4 inhibitor may be an effective therapeutic candidate for the treatment of type 2 diabetes.

• Korean Journal of Veterinary Pathology
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• v.2 no.1
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• pp.17-24
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• 1998

This is the first report of c-Jun protein expression and mRNA in a pancreatic islet in a nonobese diabetic(NOD) state mice. In this experiment NOD mice with insulin-dependent diabetes mellitus type I at age 16 weeks(n=7) just before death(n=4) were used. The control group consist of prediabetic NOD(8 weeks n=7) and ICR(8 weeks n=7 and 16 weeks n=7) mice. c-Jun positive cells in the pancreatic islet of NOD mice were localized in the same positions as a-glucagon producing cells. immunoreactivity was negative in the prediabetic NOD(8 weeks) and ICR(8 weeks and 16 weeks) mice. The number of c-Jun positive cells in mice with severe diabetic state just before death were significantly decreased when compared to NOD(16 weeks) mice. Expression of c-Jun in mRNA level was assessed by RT-PCR method. The levels of mRNA in NOD(16 weeks) mice group were elevated in total pancreatic tissues. The present results suggest that the induction of proto-oncogene protein may be of significance in assessing cell specific injury and may play a functional role between pancretic islet $\alpha$-cells and $\beta$-cells in the diabetic state.

• Journal of the East Asian Society of Dietary Life
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• v.17 no.2
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• pp.205-212
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• 2007

This study was designed to investigate a natural medicinal multi-plants extract (BG515), which consisted of multi extracts of Mori folium, Rehmannia glutinosa Liboschitz, Dioscorea japonica, Lycii fructus, and Astragalus radix, on blood glucose, insulin levels, and serum malondialdehyde (MDA) concentrations in streptozotocin-induced diabetic rats. Streptozotocin (STZ) induces a type 1 diabetes mellitus in rats. Type 1 is usually characterized by the presence of islet cell autoantibodies (ICA), autoantibodies to insulin (IAA), and autoantiboides to glutamic acid decarboxylase (GAD), which identify the autoimmune process that leads to $\beta-cell$ destruction. Thirty-five male Sprague-Dawley (SD) rats weighing $150\sim170g$ each (6 weeks old) were randomly divided into one control (Group A) and 4 STZ-induced diabetic groups, and were subjected to one of the following treatment for 12 weeks. Groups A and B were fed basal diets and Group C, D, and E received the same diets as groups A and B, but with supplements of 150 mg/kg, 300 mg/kg, and 600 mg/kg of BG515 orally for 12 weeks, respectively. Diabetes was induced in Groups B, C, D, and E by intravenous injection of 45 mg/kg of STZ per body weight in sodium citrate buffer (pH 4.5) via the tail vein. In the BG515 groups, we found increases in serum insulin levels, compared to the STZ-control group, but these data were not significant. In contrast, blood glucose and serum MDA concentrations decreased in the BG515 groups compare to the STZ-control group. At the 5th week, in all the BG515 administered groups, there were decreases in serum blood glucose levels compared to the STZ- control group, and this activity was very strong in the BG515-1 group at the 12th week. These results suggest that natural bio-complex compounds (BG515) may slightly suppress STZ-induced changes in serum MDA concentration via the maintenance of serum insulin levels, due to the prevention of $\beta-cell$ and glucagon destruction by STZ.