glycogen has been researched along with Pancreatic-Diseases* in 7 studies
1 review(s) available for glycogen and Pancreatic-Diseases
Article | Year |
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Pancreatic glucagon in health and disease.
Topics: Amino Acids; Cyclic AMP; Diabetes Mellitus; Digestive System; Fatty Acids, Nonesterified; Glucagon; Gluconeogenesis; Glucose; Glycogen; Humans; Hyperglycemia; Insulin; Insulin Secretion; Liver Glycogen; Pancreas; Pancreatic Diseases; Pancreatic Neoplasms | 1971 |
6 other study(ies) available for glycogen and Pancreatic-Diseases
Article | Year |
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Long-term High-fat High-sucrose Diet Promotes Enlarged Islets and β-Cell Damage by Oxidative Stress in Bama Minipigs.
The effect of a long-term high-fat, high-caloric diet on the dysfunction of pancreas has not been clarified. We investigated the pancreatic histopathology and β-cell apoptosis in Bama minipigs after 23 months on a high-fat high-sucrose diet (HFHSD).. Bama minipigs were randomly assigned to control (n = 6) and HFHSD groups (n = 6) for 23 months, and biochemical parameters were measured. Pancreata were subjected to histological analysis, followed by assessment with transmission electron microscopy. Lipid peroxidation was determined by the malondialdehyde concentration and antioxidant enzyme activity. Β-cell apoptosis was measured by an immunohistochemical method.. In the HFHSD group, the islets were enlarged, and the pancreatic tissue had observed significant fatty infiltration. Moreover, the feeding program damaged the normal pancreatic tissue structure. The level of lipid peroxidation was increased, and the activities of pancreatic antioxidant enzymes were significantly decreased. The expression levels of caspase-3, Bax, and insulin were significantly increased (P < 0.05), and the expression levels of proliferating cell nuclear antigen and Bcl-2 were decreased (P < 0.05).. The long-term HFHSD promotes pancreatic steatosis and oxidative stress, which increases β-cell apoptosis as indicated by the activation of caspase-3 through the mitochondrial pathway (Bcl-2/Bax). Topics: Animals; Antioxidants; Apoptosis; bcl-2-Associated X Protein; Biomarkers; Blood Glucose; Caspase 3; Cell Proliferation; Diet, High-Fat; Dietary Sucrose; Disease Models, Animal; Glycogen; Hyperinsulinism; Insulin; Insulin-Secreting Cells; Islets of Langerhans; Lipid Peroxidation; Malondialdehyde; Obesity; Oxidative Stress; Pancreatic Diseases; Proto-Oncogene Proteins c-bcl-2; Swine; Swine, Miniature; Time Factors | 2015 |
1Alpha,25 dihydroxyvitamin D3: therapeutic and preventive effects against oxidative stress, hepatic, pancreatic and renal injury in alloxan-induced diabetes in rats.
Diabetes mellitus is a major endocrine disorder and a growing health problem in most countries which can be ameliorated by numerous bio-molecules such as 1alpha,25 dihydroxyvitamin D3 [1alpha,25(OH)2VD3]. With this in mind, the current study investigated the therapeutic and preventive effects of 1alpha,25(OH)2VD3 on diabetes and its side effects: toxicity in liver, pancreas and kidneys. Our results show that administration of 1alpha,25(OH)2VD3 in diabetic rats increased the plasmatic insulin level, favored the normal blood glucose levels and normalized the hepatic glycogen concentration. In addition, 1alpha,25(OH)2VD3 enhanced superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX) (by 207, 52 and 72%, respectively) compared to diabetic rats. It also reduced lipid peroxidation and the indices of toxicity in liver and kidneys by significantly decreasing alkaline phosphatases (PAL), aspartate and lactate transaminase (AST and ALT) activities, total and direct bilirubin, triglycerides (TG), cholesterol, creatinine, urea and iron levels in diabetic rats. Moreover, the plasmatic non-enzymatic antioxidant level of HDL-cholesterol, magnesium (Mg), calcium (Ca) and copper (Cu) increased after 1alpha,25(OH)2VD3 administration. The administration of 1alpha,25(OH)2VD3 in diabetic rats protects against alloxan-induced histological changes in pancreas.. from these data, it is concluded that 1alpha,25(OH)2VD3 might be useful for the therapy and prevention of diabetes and the numerous side effects especially toxicity in liver, pancreas and kidneys and this protective effect is more obvious in our preventive experiment. Topics: Animals; Blood Glucose; Calcitriol; Catalase; Diabetes Mellitus, Experimental; Glutathione Peroxidase; Glycogen; Insulin; Kidney; Kidney Diseases; Lipid Peroxidation; Liver; Liver Diseases; Male; Organ Size; Oxidative Stress; Pancreas; Pancreatic Diseases; Rats; Rats, Wistar; Superoxide Dismutase | 2009 |
[Control of ATP levels in stimulated pancreatic B-cells].
Topics: Adenosine Triphosphate; Animals; Butyrates; Carbutamide; Cyclic AMP; Diazoxide; Epinephrine; Glucagon; Glucose; Glycogen; Histocytochemistry; Hypoglycemic Agents; In Vitro Techniques; Insulin; Insulin Secretion; Ischemia; Islets of Langerhans; Mice; Obesity; Pancreatic Diseases; Sulfonamides; Theophylline | 1969 |
[Critical choice of appropriate methods for enzymatic diagnosis of pancreatic diseases].
Topics: Amylases; Carboxypeptidases; Chymotrypsin; Duodenum; Emulsions; Glycogen; Humans; Pancreatic Diseases; Peptide Hydrolases; Trypsin | 1966 |
[Changes in the glycogen content of the kidney after application Salyrgan].
Topics: Disease; Diuretics; Glycogen; Kidney; Mersalyl; Organomercury Compounds; Pancreas; Pancreatic Diseases | 1961 |
Glycogen infiltration (hydropic degeneration) in the pancreas; a review.
Topics: Disease; Glycogen; Humans; Pancreas; Pancreatic Diseases | 1958 |