Examination of the effect of route of administration and dose on the diabetogenic effects of streptozotocin

Sweeney, C.; Redrobe, J.R; Kelly, John R.; Horrobin, David F.; Leonard, Brian E.

doi:10.1016/0378-4274(94)90347-6

Cited by 5 publications

(6 citation statements)

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“…The drug may be competing with sucrose for its substrate, and binds to -glycosidase enzymes, thus leading to inhibition of sucrose digestion (Teixeira et al, 2007). The APE had a gummy viscous appearance, thus it is possible that inhibition of intestinal glucose absorption is mediated via so called "fiber effect" (Ali et al, 1995;MacSweeney et al, 1995). This gummy appearance may be due to the presence of fibers in the APE that are known to inhibit intestinal glucose absorption (Ali et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Antihyperglycemic and hypoglycemic activities ofPhyllanthus debilisaqueous plant extract in mice

Wanniarachchi¹,

Peiris²,

Ratnasooriya³

2009

Pharmaceutical Biology

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Section: Discussionmentioning

confidence: 99%

Antihyperglycemic and hypoglycemic activities ofPhyllanthus debilisaqueous plant extract in mice

Wanniarachchi¹,

Peiris²,

Ratnasooriya³

2009

Pharmaceutical Biology

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“…The animals were divided randomly into 2 groups: control and STZ-diabetic group. Severe diabetes was induced by a single subcutaneous injection of 150 mg/kg body wt of STZ prepared fresh in 0.1 mol/L citrate buffer [21] (pH 4.5), whereas the control rats were injected with citrate buffer only. Blood glucose levels in STZ-diabetic rats were kept as close as possible to levels typical of nondiabetic animals with a twice-daily injection of a slow-acting insulin (Humulin-NPH, Eli Lilly, West Ryde, NSW, Australia) for approximately 10 days before the start of the experiments (STZ-diabetic rats received~2 units of insulin in the morning and~4.5 units of insulin in the late afternoon, whereas control animals received a physiological saline).…”

Section: Animalsmentioning

confidence: 99%

Effect of impaired glucose uptake on postexercise glycogen repletion in skeletal muscles of insulin-treated streptozotocin-diabetic fasted rats

Ferreira

Palmer

et al. 2005

Metabolism

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“…STZ administered subcutaneously (s.c.) produces diabetes more consistently than by intraperitoneal (i.p.) administration (MacSweeney et al, 1995). Rats to be rendered diabetic were fasted overnight, anesthetized under 5% isoflurane-95% oxygen for 1 min, and injected s.c. with 50 mg/kg STZ (Sigma, St. Louis, MO) in 10 mM sodium citrate and 0.9% NaCl, pH 4.5.…”

Section: Diabetic Rat Treatmentmentioning

confidence: 99%

Systemic insulin‐like growth factor‐I administration prevents cognitive impairment in diabetic rats, and brain IGF regulates learning/memory in normal adult rats

Lupien¹,

Bluhm²,

Ishii³

2003

J of Neuroscience Research

132

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Diabetic patients have impaired learning/memory, brain atrophy, and two-fold increased risk of dementia. The cause of cognitive disturbances that progress to dementia is unknown. Because neurotrophic insulin-like growth factor (IGF) levels are reduced in diabetic patients and rodents, and IGF can cross the blood-central nervous system barrier (B-CNS-B), the hypothesis was tested that IGF administered systemically can prevent cognitive disturbances, independently of hyperglycemia and a generalized catabolic state. Latency to escape to a hidden platform in the Morris Water Maze is used widely to test spatial memory, a hippocampus-dependent task. Adult rats were rendered diabetic with streptozotocin and implanted 4 weeks later with subcutaneous pumps that released either vehicle (D + Veh) or 20 microg/day IGF-I (D + IGF). Latency to escape to the hidden platform was prolonged in (D + Veh) versus non-diabetic rats (P < 0.003) 10.5 weeks after the onset of diabetes. Such prolongation was prevented in (D + IGF) versus (D + Veh) rats (P < 0.03). The data show that IGF-I can act across the B-CNS-B to prevent loss of cognition-related performance in the water maze independently of ongoing hyperglycemia and reduction in brain (P < 0.001) and whole body weight (P < 0.001) in diabetic rats. The hypothesis that brain IGF contributes to learning/memory was tested. An anti-IGF antibody, or preimmune serum, was infused into the lateral ventricles in non-diabetic rats. Learning in a passive avoidance task was impaired significantly in the IGF antibody versus preimmune serum-treated groups on test Days 1, 2, and 3 (P = 0.04, 0.02 and 0.004, respectively). The data together are consistent with a model in which brain IGF is essential for learning/memory, and a loss of IGF activity due to diabetes may contribute to cognitive disturbances.

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Examination of the effect of route of administration and dose on the diabetogenic effects of streptozotocin

Cited by 5 publications

References 0 publications

Antihyperglycemic and hypoglycemic activities ofPhyllanthus debilisaqueous plant extract in mice

Antihyperglycemic and hypoglycemic activities ofPhyllanthus debilisaqueous plant extract in mice

Effect of impaired glucose uptake on postexercise glycogen repletion in skeletal muscles of insulin-treated streptozotocin-diabetic fasted rats

Systemic insulin‐like growth factor‐I administration prevents cognitive impairment in diabetic rats, and brain IGF regulates learning/memory in normal adult rats

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