[ Diabetes Solutions ]

ob/ob mouse

Description: PNAS is the world’s most-cited multidisciplinary scientific serial. Type I diabetes is an autoimmune disease resulting from the specific destruction of the insulin-producing pancreatic beta-cells. Autoimmune insulitis, hypoinsulinemia, glycosuria, and hyperglycemia characterize diabetes in NOD/LtJ mice. That condition is a leading cause of birth defects and can predispose the child to develop diabetes later in life. MICE or PRODUCTS shall not be: (i) used for any purpose other than internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Our preliminary studies support our proposal and suggest that this longitudinal in vivo imaging will provide insight into key events in the islet. Although the increased death rate is mainly due to cardiovascular disease, deaths from non-cardiovascular causes are also increasing [34].

For example, if the current year is 2008 and a journal has a 5 year moving wall, articles from the year 2002 are available. Zhou and colleagues recently demonstrated that thapsigargin-induced apoptosis in the MIN6 pancreatic β-cell line was significantly attenuated by lipoxygenase inhibitors. Data from animal experiments should first be interpreted in ways that are compatible with, and if possible explain, what is known to happen in human experiments and in observed clinical practice. Consistent with the requirement for a written understanding regarding animal care and use, the JACKSON Animal Care and Use Committee will review the animal care and use protocol(s) associated with any SERVICES to be performed at JACKSON, and JACKSON shall have ultimate responsibility and authority for the care of animals while on site or in JACKSON custody. (h) Electron photomicrographs of kidneys from STZ-treated CKO and control mice. “The physiology of obese-hyperglycemic mice [ob/ob mice]”. The results of these studies now define a new, negatively regulated substrate of the insulin signaling pathway specifically within beta-cells that when elevated, can impair replication and increase apoptosis, resulting in loss of beta-cells and diabetes.

7: 666–85. They arrived at this conclusion when they found that mice lacking FGF1, when put on a high-fat diet, quickly developed diabetes. PMID 17619751. ^ Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (December 1994). “Positional cloning of the mouse obese gene and its human homologue”. Nature. 372 (6505): 425–32.

doi:10.1038/372425a0. PMID 7984236. ^ Friedman JM, Halaas JL (October 1998). & Owen, S. Nature. 395 (6704): 763–70. doi:10.1038/27376.

PMID 9796811.

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