Quantitative immunogold study of glucose transporter (GLUT-1) in five brain regions of scrapie-infected mice showing obesity and reduced glucose tolerance

Aw, Vorbrodt; Dh, Dobrogowska; Tarnawski, Michał; Meeker, Harry C.; Ri, Carp

doi:10.1007/s004010100382

Cited by 19 publications

(4 citation statements)

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“…On the other hand, the decrease in GLUT1 expression in the hypothalamus, 22 thalamus, cerebellum and hippocampus, mediated by high glucose levels has been described. 23 Similar to our ndings, Hou et al 24 demonstrated decreased GLUT1 and GLUT3 expression in the brain of diabetic rats, with transporter levels being negatively correlated with blood glucose. However, it is important to mention that all studies cited above measured mostly GLUT1 and GLUT3 mRNA that may not always be translated into the protein content.…”

Section: Paper 2 Resultssupporting

confidence: 89%

Chronic sulforaphane oral treatment accentuates blood glucose impairment and may affect GLUT3 expression in the cerebral cortex and hypothalamus of rats fed with a highly palatable diet

Souza¹,

Riboldi²,

Hansen³

et al. 2013

Food Funct.

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Obesity and insulin resistance are the key factors underlying the etiology of major health problems such as hypertension, diabetes and stroke. These important health issues lead researchers to investigate new approaches to prevent and treat obesity and insulin resistance. Good candidates are the phytochemical compounds that have been extensively studied in the field. Therefore, the aim of this study was to test whether sulforaphane (SFN, 1 mg kg⁻¹, 4 months treatment), a potent inducer of antioxidant enzymes present in cruciferous vegetables, had some beneficial effects on obesity and insulin resistance induced by a highly palatable (HP) diet in male Wistar rats. Glucose tolerance, serum and hepatic lipid levels, lipid profile, ALT, AST, urea and creatinine, GLUT1 and GLUT3 levels in the cerebral cortex, hippocampus and hypothalamus were analyzed. Glucose tolerance was lower in the HP diet groups, especially in the HP group treated with SFN. Except for the liver triacylglycerols, no differences were found in serum lipids, hepatic and kidney markers of the HP diet groups. Although expression of GLUT1 was similar between groups for all three brain structures analyzed, expression of GLUT3 in the cortex and hypothalamus had a tendency to decrease in the HP diet group treated with SFN. In conclusion, SFN at the specific dose was able to accentuate glucose intolerance and may affect GLUT3 expression in the cerebral cortex and hypothalamus.

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Section: Paper 2 Resultssupporting

confidence: 89%

Chronic sulforaphane oral treatment accentuates blood glucose impairment and may affect GLUT3 expression in the cerebral cortex and hypothalamus of rats fed with a highly palatable diet

Souza¹,

Riboldi²,

Hansen³

et al. 2013

Food Funct.

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“…The concept of virus‐induced obesity is not new. There have been eight different viruses that are reported to produce obesity in animals 26–37, 39–87. Lyons et al 26 published the first report of virus‐induced obesity in 1982, showing that canine distemper virus produced obesity in surviving infected mice.…”

Section: Increase In Visceral Fat and Prevalence Of Obesity In Animalmentioning

confidence: 99%

“…Three more viruses were reported to produce obesity in animals by damaging the CNS 39–70. Rous‐associated virus type 7 (RAV‐7) was found to cause obesity in chickens 39, 40.…”

Section: Increase In Visceral Fat and Prevalence Of Obesity In Animalmentioning

confidence: 99%

“…The ME‐7 strain of scrapie produced obesity in mice, but other scrapie strains did not 58, 59. Reports of pancreatic damage by the scrapie agent leading to diabetes are numerous 60–69. Removal of the adrenal gland prevented obesity, so Kim et al 59 postulated that the hypothalamic‐pituitary‐adrenal axis (HPA) is necessary for the development of obesity.…”

Section: Increase In Visceral Fat and Prevalence Of Obesity In Animalmentioning

confidence: 99%

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Could viruses contribute to the worldwide epidemic of obesity?

Atkinson¹

2008

International Journal of Pediatric Obesity

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The prevalence of obesity in children increased rapidly starting about 1980 in both developed and developing countries. Studies of changes in diet and physical activity, television watching, and food advertisements on television suggest that these are not sufficient to explain the epidemic. The pattern of rapid spread is suggestive of an infectious origin. The concept of virus-induced obesity is not new. Eight viruses have been shown to cause obesity in animals and there is evidence for virus-induced obesity in humans. Recent evidence on animal and human adenoviruses suggests that these adenoviruses may infect adipocytes to alter enzymes and transcription factors resulting in accumulation of triglycerides and differentiation of preadipocytes into mature adipocytes. The E4orf1 gene of Ad-36 has been shown to be responsible for the adipogenic effect. It appears that a portion of the worldwide epidemic of obesity since 1980 could be due to infections with human adenoviruses.

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