Resistin expression and regulation in mouse pituitary

AbstractResistin, a new adipocytokine, is expressed in human, rat and mouse adipose tissue. Its putative role as a mediator of insulin resistance is controversial. We hypothesized that resistin, in common with leptin, has multiple roles in non-adipose tissues. Using reverse transcription polymerase chain reaction (RT-PCR) we show that the resistin gene (Retn) is expressed in mouse brain (hypothalamus and cortex) and pituitary gland. Immunohistochemistry revealed resistin protein in the arcuate nucleus and pituitary gland. Semi-quantitative RT-PCR analysis indicated that Retn mRNA is developmentally regulated in the pituitary. Expression was lowest at birth, increased abruptly between postnatal days 14 and 25 (four-fold; P<0.001), and declined thereafter. This peak in pituitary Retn mRNA was unaffected by early weaning but was abolished by neonatal treatment with monosodium glutamate, suggesting that the basal hypothalamus regulates pituitary Retn. Although the role(s) of endogenous resistin in mouse brain and pituitary remains to be determined, it may be distinct from its controversial involvement in insulin resistance. Our data suggest that local resistin expression could have functional implications during prepubertal maturation of the hypothalamic–pituitary system

Anemia is an independent risk for mortality after acute myocardial infarction in patients with and without diabetes

INTRODUCTION: Anemia and diabetes are risk factors for short-term mortality following an acute myocardial infarction(AMI). Anemia is more prevalent in patients with diabetes. We performed a retrospective study to assess the impact of the combination of diabetes and anemia on post-myocardial infarction outcomes. METHODS: Data relating to all consecutive patients hospitalized with AMI was obtained from a population-based disease-specific registry. Patients were divided into 4 groups: diabetes and anemia (group A, n = 716), diabetes and no anemia (group B, n = 1894), no diabetes and anemia (group C, n = 869), and no diabetes and no anemia (group D, n = 3987). Mortality at 30 days and 31 days to 36 months were the main outcome measures. RESULTS: 30-day mortality was 32.3% in group A, 16.1% in group B, 21.5% in group C, 6.6% in group D (all p < 0.001). 31-day to 36-month mortality was 47.6% in group A, 20.8% in group B, 34.3% in group C, and 10.4% in group D (all p < 0.001). Diabetes and anemia remained independent risk factors for mortality with odds ratios of 1.61 (1.41–1.85, p < 0.001) and 1.59 (1.38–1.85, p < 0.001) respectively at 36 months. Cardiovascular death from 31-days to 36-months was 43.7% of deaths in group A, 54.1% in group B, 47.0% in group C, 50.8% group D (A vs B, p < 0.05). INTERPRETATION: Patients with both diabetes and anemia have a significantly higher mortality than those with either diabetes or anemia alone. Cardiovascular death remained the most likely cause of mortality in all groups