Browsing by Subject "Diabetes mellitus"

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Neuroprotective effects of peroxisome proliferator-activated receptor-gamma (PPAR-y) ligands against oxidative stress
(2003-12-01) Aoun, Paul; Simpkins, James W.; Dillon, Glenn; Gracy, Robert
Aoun, Paul Neuroprotective effects of peroxisome proliferator-activated receptor-gamma (PPAR-y) ligands against oxidative stress. Doctor of Philosophy (Pharmacology and Neurosciences), December, 2003, 254 pp., 37 figures. Diabetes mellitus is a significant public health problem in the United States and the world resulting in substantial morbidity and mortality. Diabetes complications, i.e., neuropathy, are common and almost triple the annual cost of managing diabetes. In our studies, we investigated the role that insulin sensitizers currently used for the treatment of diabetes, the PPAR-y ligands, might play in protecting neurons against oxidative stresses. We showed that two PPAR-y ligands, 15 deoxy-PGJ2 and troglitazone, protected, in a dose-dependent manner, HT-22 mouse hippocampal and RGC-5 retinal ganglion cell lines against various oxidative insults. Further, we demonstrated that neuroprotection by 15deoxy-PGJ2 and troglitazone was independent of the PPAR-y receptor. Our findings brought to light an important role of PPAR-y ligands in preventing neuronal complications from diabetes. Moreover, the studies reported herein provide valuable insights into the development of novel therapeutic compounds that improve insulin sensitivity while preventing neurological, and possibly other complications of diabetes.
Regional Adipose Tissue Deposition, Its Rate of Lipolysis, and Subsequent Effect of Insulin Resistance-in Type II Diabetes Mellitus
(1999-06-01) Schalscha, Alan G.; Raven, Peter B.; Downey, H. Fred; Caffrey, James L.
Diabetes mellitus is a disease that plagues populations world wide. More than 5 percent of U.S. citizens are afflicted with one or another form of this disease (22). This paper begins by discussing the incidence of this illness as it affects Americans. An explanation of the four forms in which diabetes mellitus itself will be offered, and these will be classified according to etiology. Non-insulin dependent diabetes mellitus (NIDDM), also called type II diabetes mellitus, will be the last of these forms mentioned. Due to its prevalence, NIDDM will be the focus of this paper. The proposed pathophysiology of NIDDM will be discussed, though to researchers it still remains somewhat of a mystery. This paper will then briefly the genetic and environmental interaction responsible for the onset of non-insulin dependent diabetes mellitus. A brief discussion of the interrelationship between decreasing physical activity and a subsequent increase in obesity will follow (38). The location of adipose tissue seems to have adverse effects on certain aspects of NIDDM, including its sensitivity to insulin. This paper proposes that either subcutaneous or visceral adipose deposits specifically reduce insulin sensitivity more than other fat stores. The connection between adipose tissue and insulin sensitivity appears to be mediated by fatty acids released from specific depots and their destination immediately following release.