Involvement of ASK1-p38 pathway in the pathogenesis of diabetes triggered by pancreatic ß cell exhaustion.

Background: Diabetes mellitus is characterized by high blood glucose levels. Pancreatic ß cell death contributes to type 1 and type 2 diabetes. Akita mice, which harbor a human permanent neonatal diabetes-linked mutation (Cys96Tyr) in the insulin gene, are well established as an animal model of diabetes caused by pancreatic ß cell exhaustion.

Thioredoxin suppresses Parkin-associated endothelin receptor-like receptor-induced neurotoxicity and extends longevity in Drosophila.

Parkin-associated endothelin receptor-like receptor (Pael-R) is a substrate of the E3 ubiquitin ligase Parkin, which has been implicated in the pathogenesis of Parkinson disease. Misexpression of human Pael-R in Drosophila has been shown to induce selective loss of dopaminergic neurons, a symptom of Parkinson disease. Using this model, we investigated whether thioredoxin (TRX), an evolutionarily conserved antioxidant and molecular chaperone, could suppress the neurotoxicity induced by Pael-R.

Non-traumatic recurrent dissection and its spontaneous repair in the circle of Willis: report of two autopsy cases.

Post-mortem examinations of the circle of Willis in two cases of subarachnoid hemorrhage disclosed a wide spectrum of vasculopathy ranging from a minimal tear between the intima and media, and between the media and adventitia, to complete transmural disruption leading to the formation of pseudoaneurysms. The presence of coexistence of the focal lesions with complete replacement of the entire arterial wall with thick fibrous connective tissues and the vasculopathy was suggestive of the spontaneous repair of recurrent non-traumatic dissection of intracranial arteries. The patients were 58-year-old and 43-year-old females.

Effects of a high-sucrose diet on body weight, plasma triglycerides, and stress tolerance.

We examine the effects of feeding a high-sucrose diet on body weight gain, plasma triglycerides, and stress tolerance in rats. Feeding a high-sucrose (60%) diet for 2 weeks did not induce a greater body weight gain compared with that of standard diet when caloric intake was similar in ventromedial hypothalamic-lesioned obese and sham-operated lean animals. The high-sucrose diet elevated plasma triglycerides by increasing the triglyceride secretion rate and decreasing the fractional catabolic rate in both groups.

Fasting increases gene expressions of uncoupling proteins and peroxisome proliferator-activated receptor-gamma in brown adipose tissue of ventromedial hypothalamus-lesioned rats.

Uncoupling proteins (UCPs) are supposed to be involved in diet-induced thermogenesis. Their activities are usually elevated by feeding and reduced by fasting in normal animals. To investigate whether fasting affects the expression of UCPs mRNA in brown adipose tissue (BAT) of bilateral ventromedial hypothalamus (VMH)-lesioned rats, we determined the gene expression of UCP1, UCP2 or UCP3 in BAT of VMH-lesioned rats and examined oxygen consumption in these rats under fed or 48-h fasted conditions.

Distinct role of adiposity and insulin resistance in glucose intolerance: studies in ventromedial hypothalamic-lesioned obese rats.

It remains unclear whether adiposity plays an important role in glucose intolerance independently of insulin resistance. We investigated whether adiposity and insulin resistance had distinct roles in glucose intolerance in rats. We examined glucose tolerance and insulin resistance using ventromedial hypothalamic (VMH)-lesioned rats in the dynamic and the static phases of obesity (2 and 14 weeks after lesioning, respectively).