scholarly journals Effects of Low-Dose Prednisolone on Hepatic and Peripheral Insulin Sensitivity, Insulin Secretion, and Abdominal Adiposity in Patients With Inflammatory Rheumatologic Disease

Diabetes Care ◽  
2013 ◽  
Vol 36 (9) ◽  
pp. 2822-2829 ◽  
Author(s):  
Carolyn J. Petersons ◽  
Brenda L. Mangelsdorf ◽  
Arthur B. Jenkins ◽  
Anne Poljak ◽  
Malcolm D. Smith ◽  
...  
Diabetes ◽  
2013 ◽  
Vol 63 (5) ◽  
pp. 1725-1737 ◽  
Author(s):  
Kirstine N. Bojsen-Møller ◽  
Carsten Dirksen ◽  
Nils B. Jørgensen ◽  
Siv H. Jacobsen ◽  
Annette K. Serup ◽  
...  

1989 ◽  
Vol 75 (2-3) ◽  
pp. 175-181 ◽  
Author(s):  
G. Riccardi ◽  
S. Genovese ◽  
G. Saldalamacchia ◽  
L. Patti ◽  
G. Marotta ◽  
...  

Author(s):  
Eva Tudurí ◽  
Sergi Soriano ◽  
Lucía Almagro ◽  
Anabel García-Heredia ◽  
Alex Rafacho ◽  
...  

Abstract Aging is associated with a decline in peripheral insulin sensitivity and an increased risk of impaired glucose tolerance and type 2 diabetes. During conditions of reduced insulin sensitivity, pancreatic β-cells undergo adaptive responses to increase insulin secretion and maintain euglycemia. However, the existence and nature of β-cell adaptations and/or alterations during aging are still a matter of debate. In this study, we investigated the effects of aging on β-cell function from control (3-month-old) and aged (20-month-old) mice. Aged animals were further categorized in two groups: high insulin sensitive (aged-HIS) and low insulin sensitive (aged-LIS). Aged-LIS mice were hyperinsulinemic, glucose intolerant and displayed impaired glucose-stimulated insulin and C-peptide secretion, whereas aged-HIS animals showed characteristics in glucose homeostasis similar to controls. In isolated β-cells, we observed that glucose-induced inhibition of KATP channel activity was reduced with aging, particularly in the aged-LIS group. Glucose-induced islet NAD(P)H production was decreased in aged mice, suggesting impaired mitochondrial function. In contrast, voltage-gated Ca 2+ currents were higher in aged-LIS β-cells, and pancreatic islets of both aged groups displayed increased glucose-induced Ca 2+ signaling and augmented insulin secretion compared with controls. Morphological analysis of pancreas sections also revealed augmented β-cell mass with aging, especially in the aged-LIS group, as well as ultrastructural β-cell changes. Altogether, these findings indicate that aged mouse β-cells compensate for the aging-induced alterations in the stimulus-secretion coupling, particularly by adjusting their Ca 2+ influx to ensure insulin secretion. These results also suggest that decreased peripheral insulin sensitivity exacerbates the effects of aging on β-cells.


2015 ◽  
Vol 309 (5) ◽  
pp. E466-E473 ◽  
Author(s):  
Robert H. J. Bandsma ◽  
Cameron Ackerley ◽  
Khajag Koulajian ◽  
Ling Zhang ◽  
Tim van Zutphen ◽  
...  

Severe malnutrition is a leading cause of global childhood mortality, and infection and hypoglycemia or hyperglycemia are commonly present. The etiology behind the changes in glucose homeostasis is poorly understood. Here, we generated an animal model of severe malnutrition with and without low-grade inflammation to investigate the effects on glucose homeostasis. Immediately after weaning, rats were fed diets containing 5 [low-protein diet (LP)] or 20% protein [control diet (CTRL)], with or without repeated low-dose intraperitoneal lipopolysaccharide (LPS; 2 mg/kg), to mimic inflammation resulting from infections. After 4 wk on the diets, hyperglycemic clamps or euglycemic hyperinsulinemic clamps were performed with infusion of [U-13C6]glucose and [2-13C]glycerol to assess insulin secretion, action, and hepatic glucose metabolism. In separate studies, pancreatic islets were isolated for further analyses of insulin secretion and islet morphometry. Glucose clearance was reduced significantly by LP feeding alone (16%) and by LP feeding with LPS administration (43.8%) compared with control during the hyperglycemic clamps. This was associated with a strongly reduced insulin secretion in LP-fed rats in vivo as well as ex vivo in islets but signficantly enhanced whole body insulin sensitivity. Gluconeogenesis rates were unaffected by LP feeding, but glycogenolysis was higher after LP feeding. A protein-deficient diet in young rats leads to a susceptibility to low-dose endotoxin-induced impairment in glucose clearance with a decrease in the islet insulin secretory pathway. A protein-deficient diet is associated with enhanced peripheral insulin sensitivity but impaired insulin-mediated suppression of hepatic glycogenolysis.


Sign in / Sign up

Export Citation Format

Share Document