ABSTRACT
Diabetes and obesity are both increasing dramatically in the United States of America and other parts of the world. One third of the American population (34%) are obese (BMI >30 kg/m2). Eleven percent of the population over 20 years of age have type 2 diabetes. Significant increases are predicted by 2050, which is significant because both diabetes and obesity are independent risk factors for hosts of other diseases, as well as risk factors for each other. These conditions constitute major sources of morbidity and mortality, as well as financial loss through impairment of abilities to work, and by creating and exaggerating disease leading to increased expense of healthcare, and increased need in frequency of healthcare. T-Bet Transcription Factor is one mechanism linking both diabetes and obesity interaction. Particular T-Bet genotypes result in varied body-type (mass/obesity) to insulin sensitivity profiles. Lipotoxicity is another linking factor between obesity and type 2 diabetes mellitus. Visceral adiposity accelerates development of insulin resistance by causing chronic increase in fatty acids in circulation, causing reduction in usage of glucose as a cellular energy source. Central obesity is particularly disposing to this kind of insulin resistance development. Cytokine, adipokines including tumor necrosis factor, IL-6, resisitin, retinol binding protein 4 and others are linked in development of insulin resistance as well. Mitochondrial dysfunction has also been identified as a factor in the correlation between these 2 diseases. Causal genes such as PPARG, KCNJ11, melanocortin-4 gene, TCF7L2 variants and others are also implicated and are actively being investigated further to elucidate complexities of these mechanisms and allow for therapeutic interventional opportunities in the future.
ABSTRACT
BACKGROUND: Hyponatremia develops in approximately a third of patients with aneurysmal subarachnoid hemorrhage (SAH). Studies have been conflicting about the association between hyponatremia and cerebrovascular spasm (CVS). AIMS: To investigate whether hyponatremia can signal the onset of CVS. SETTINGS AND DESIGN: Retrospective chart review of all patients with SAH treated at a tertiary-care university hospital from January to May 2002. MATERIALS AND METHODS: 106 patients were included in the study. Serum sodium levels were recorded from days 1 to 14 of hospitalization. Hyponatremia was defined as serum sodium level<135 meq/l and a fall in sodium level of >4 meq/l from the admission sodium level. The presence of CVS was determined by transcranial doppler sonography. Patients were assigned to one of four groups based on the presence or absence of CVS and hyponatremia. STATISTICAL ANALYSIS: Student's t-test was used for comparison of means. A logistical regression model was constructed and odds ratios (OR) were calculated. RESULTS: 41 patients developed hyponatremia and 44 developed CVS. Among the 41 with hyponatremia, 22 (54%) had evidence of CVS, whereas among the 65 patients without hyponatremia, 22 (34%) had evidence of CVS (P=0.023). Among those with hyponatremia, the mean sodium drop was 7.9 meq/L in those with CVS compared to 7.0 meq/L in those without CVS (P=0.068). More than half of those with hyponatremia and CVS (13/22) developed hyponatremia at least a day before CVS was diagnosed. CONCLUSION: In patients with SAH, hyponatremia is associated with a significantly greater risk of developing CVS and may precede CVS by at least one day.