Western diet-induced obesity results in brain mitochondrial dysfunction in female Ossabaw swine.

Diet-induced obesity is implicated in the development of a variety of neurodegenerative disorders. Concurrently, the loss of mitochondrial Complex I protein or function is emerging as a key phenotype across an array of neurodegenerative disorders. Therefore, the objective of this study was to determine if Western diet (WD) feeding in swine [carbohydrate = 40.8% kCal (17.8% of total calories from high fructose corn syrup), protein = 16.2% kcal, fat = 42.9% kCal, and 2% cholesterol] would result in Complex I syndrome pathology. To characterize the effects of WD-induced obesity on brain mitochondria in swine, high resolution respirometry measurements from isolated brain mitochondria, oxidative phosphorylation Complex expression, and indices of oxidative stress and mitochondrial biogenesis were assessed in female Ossabaw swine fed a WD for 6-months. In line with Complex I syndrome, WD feeding severely reduced State 3 Complex I, State 3 Complex I and II, and uncoupled mitochondrial respiration in the hippocampus and prefrontal cortex (PFC). State 3 Complex I mitochondrial respiration in the PFC inversely correlated with serum total cholesterol. WD feeding also significantly reduced protein expression of oxidative phosphorylation Complexes I-V in the PFC. WD feeding significantly increased markers of antioxidant defense and mitochondrial biogenesis in the hippocampi and PFC. These data suggest WD-induced obesity may contribute to Complex I syndrome pathology by increasing oxidative stress, decreasing oxidative phosphorylation Complex protein expression, and reducing brain mitochondrial respiration. Furthermore, these findings provide mechanistic insight into the clinical link between obesity and mitochondrial Complex I related neurodegenerative disorders.

Epidemiology of death from aneurysmal subarachnoid hemorrhage in New Mexico.

BACKGROUND: The authors report the first retrospective analysis of all reported cases of death from aneurysmal subarachnoid hemorrhage in the state of New Mexico from 1 January 2001 to 31 December 2007. METHODS: Data were obtained from the New Mexico Vital Records and Health Statistics Department in Santa Fe, New Mexico. RESULTS: The incidence of death from aneurysmal subarachnoid hemorrhage in the state of New Mexico is 2.96/100,000 people per year. Each cultural subgroup and various risk factors in these patients were further analyzed. CONCLUSIONS: This report represents the first documented review of death from aneurysmal subarachnoid hemorrhage in the state of New Mexico. There was a lower incidence in New Mexico compared with the national average. Cultural breakdowns and associated epidemiological factors are discussed.