scholarly journals Insulin-independent promotion of chemically induced hepatocellular tumor development in genetically diabetic mice

2010 ◽  
Vol 101 (1) ◽  
pp. 65-72 ◽  
Author(s):  
Kohtaro Yamasaki ◽  
Yoshihiro Hayashi ◽  
Sumika Okamoto ◽  
Makoto Osanai ◽  
Gang-Hong Lee
2011 ◽  
Vol 81 (1) ◽  
pp. 34-42 ◽  
Author(s):  
Joel Deneau ◽  
Taufeeq Ahmed ◽  
Roger Blotsky ◽  
Krzysztof Bojanowski

Type II diabetes is a metabolic disease mediated through multiple molecular pathways. Here, we report anti-diabetic effect of a standardized isolate from a fossil material - a mineraloid leonardite - in in vitro tests and in genetically diabetic mice. The mineraloid isolate stimulated mitochondrial metabolism in human fibroblasts and this stimulation correlated with enhanced expression of genes coding for mitochondrial proteins such as ATP synthases and ribosomal protein precursors, as measured by DNA microarrays. In the diabetic animal model, consumption of the Totala isolate resulted in decreased weight gain, blood glucose, and glycated hemoglobin. To our best knowledge, this is the first description ever of a fossil material having anti-diabetic activity in pre-clinical models.


Diabetes ◽  
1985 ◽  
Vol 34 (11) ◽  
pp. 1075-1081 ◽  
Author(s):  
T. H. Kuo ◽  
F. Giacomelli ◽  
J. Wiener ◽  
K. Lapanowski-Netzel

Diabetes ◽  
1983 ◽  
Vol 32 (9) ◽  
pp. 781-787 ◽  
Author(s):  
T. H. Kuo ◽  
K. H. Moore ◽  
F. Giacomelli ◽  
J. Wiener

1987 ◽  
Vol 253 (3) ◽  
pp. R516-R522 ◽  
Author(s):  
J. E. Morley ◽  
E. N. Hernandez ◽  
J. F. Flood

Neuropeptide Y (NPY) stimulates eating in a number of species. In the studies reported here, intracerebroventricular administration of porcine NPY increased eating in mice. In the presence of food, NPY caused enhancement of water intake, whereas in the absence of food, NPY suppressed water intake. Behavioral analysis showed that NPY decreased the latency to eat, increased the time spent eating, and decreased grooming. Human NPY also increased food intake, whereas the free acid of NPY was inactive. Although some minor discrepancies in response were noted overall, NPY was as effective at stimulating food intake in genetically obese (ob/ob) mice compared with their lean littermates (ob/-), in genetically diabetic mice (db/db) and their nondiabetic heterozygote control (db/m), in streptozocin-induced diabetic mice and their controls, and in adult (8 mo old) compared with old (25 mo old) mice.


2010 ◽  
Vol 22 (2) ◽  
pp. 61-67 ◽  
Author(s):  
Daichi Chikazu ◽  
Tetsushi Taguchi ◽  
Hiroyuki Koyama ◽  
Hisako Hikiji ◽  
Hisako Fujihara ◽  
...  

2014 ◽  
Vol 171 (9) ◽  
pp. 2300-2307 ◽  
Author(s):  
Alessandra Bitto ◽  
Domenica Altavilla ◽  
Gabriele Pizzino ◽  
Natasha Irrera ◽  
Giovanni Pallio ◽  
...  

2020 ◽  
Vol 21 (23) ◽  
pp. 9295
Author(s):  
Nadine Brandes ◽  
Slavica Hristomanova Mitkovska ◽  
Dominik Simon Botermann ◽  
Wiebke Maurer ◽  
Anna Müllen ◽  
...  

Basal cell carcinoma (BCC) originate from Hedgehog/Patched signaling-activated epidermal stem cells. However, the chemically induced tumorigenesis of mice with a CD4Cre-mediated biallelic loss of the Hedgehog signaling repressor Patched also induces BCC formation. Here, we identified the cellular origin of CD4Cre-targeted BCC progenitors as rare Keratin 5+ epidermal cells and show that wildtype Patched offspring of these cells spread over the hair follicle/skin complex with increasing mouse age. Intriguingly, Patched mutant counterparts are undetectable in age-matched untreated skin but are getting traceable upon applying the chemical tumorigenesis protocol. Together, our data show that biallelic Patched depletion in rare Keratin 5+ epidermal cells is not sufficient to drive BCC development, because the spread of these cells is physiologically suppressed. However, bypassing the repression of Patched mutant cells, e.g., by exogenous stimuli, leads to an accumulation of BCC precursor cells and, finally, to tumor development.


1980 ◽  
Vol 238 (5) ◽  
pp. G419-G423 ◽  
Author(s):  
R. Bennetts ◽  
K. Ramaswamy

Na+-dependent D-glucose and L-leucine uptakes by isolated small intestinal brush-border membrane vesicles were studied in normal and genetically diabetic mice (C57BL/KsJ-dbm). Vesicles from normal mice demonstrated transport characteristics and morphological appearances identical to those from other mammalian small intestinal brush-border membrane isolates. There was no difference found between genetically diabetic mice and their littermate controls. These data suggest that the small intestinal brush-border membrane transport is not altered in genetic diabetes in contrast to that found in drug-induced diabetes.


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