During the past decade a number of investigators have attempted to develop mouse models of diabetic macrovascular disease. Hyperglycemia might increase vascular damage because it increases oxidant stress. For this reason we studied animals that were deficient in HDL; HDL is widely believed to protect against oxidant stress. An inbred line of mice doubly deficient in LDL receptor and apoAI was made diabetic with streptozotocin (STZ); control mice had an average glucose of 7.2+/-2mmol/l and STZ-treated mice had an average glucose of 19.4+/-6.5mmol/l. The animals were fed a high cholesterol but low fat diet leading to plasma cholesterol levels of 9.4+/-1.6mmol/l in control animals and 10.1+/-1.8mmol/l in STZ-treated mice. The control and STZ-treated animals had similar plasma lipoprotein profiles. Atherosclerosis assessed at 23 weeks averaged 38154microm(2) in control and 32962microm(2) in STZ-treated mice. Therefore STZ-induced diabetes does not alter plasma lipoproteins or atherosclerosis in HDL deficient mice.
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http://dx.doi.org/10.1016/j.atherosclerosis.2003.09.014 | DOI Listing |
PLoS One
October 2024
Department of Medicine, McGill University Health Centre, McGill University, Montreal, Quebec, Canada.
Redox Biol
December 2024
Guangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Guangzhou, 510080, Guangdong, PR China; Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, PR China. Electronic address:
Statins therapy is efficacious in diminishing the risk of major cardiovascular events in diabetic patients. However, our research has uncovered a correlation between the prolonged administration of statins and an elevated risk of myocardial dysfunction in patients with type II diabetes mellitus (TIIDM). Here, we report the induction of sterol regulatory element-binding protein 1 (SREBP1) activation, associated lipid peroxidation, and the consequent diabetic myocardial dysfunction after statin treatment and explored the underlying mechanisms.
View Article and Find Full Text PDFInt J Mol Sci
October 2024
Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, London, ON N6A 3K7, Canada.
Following the near-total depletion of pancreatic beta-cells with streptozotocin (STZ), a partial recovery of beta-cell mass (BCM) can occur, in part due to the alpha- to beta-cell transdifferentiation with an intermediary insulin/glucagon bi-hormonal cell phenotype. However, human type 2 diabetes typically involves only a partial reduction in BCM and it is not known if recovery after therapeutic intervention involves islet cell transdifferentiation, or how this varies with age. Here, we used transgenic mouse models to examine if islet cell transdifferentiation contributes to BCM recovery following only a partial depletion of BCM.
View Article and Find Full Text PDFInt J Mol Sci
September 2024
Department of Physiology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Phytomedicine
December 2024
Department of Clinical Medicine, Affiliated Hospital of Hangzhou Normal University, Hangzhou Normal University, Hangzhou, 310000, PR China. Electronic address:
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