Monday, June 17, 2013

Good Stuff

Okay people. Despite the fact that it's 450 pages of geekspeak and I have puppy-on-the-brain, I went out and looked through the abstracts from the Sleep conference (link).
Ironically, I scrolled randomly and this is the first study I landed on:
0015  Absence of the hypocretin peptide increases serum insulin without altering blood glucose or serum leptin levels in aged male mice.      Ramanathan L, Siegel J
Introduction: We previously reported that both male and female Hcrt deficient mice showed increased body fat, although only the female mice showed increased body weight, compared to gender and genotype matched wildtype (WT) controls. In this study we compared blood glucose and serum leptin and insulin levels in male Hcrt deficient and WT mice. We also analyzed changes in the weight of the brain, heart, liver, spleen, pancreas, kidney, thymus, lungs, testes, bladder and stomach of these mice.
Results: Blood glucose levels were not significantly different between male Hcrt deficient and WT mice. However, male Hcrt deficient mice had significantly higher serum insulin levels compared to WT controls (129%, p= 0.02). Although serum leptin levels were higher in male Hcrt deficient mice compared to WT mice, this difference was not significant (. Furthermore, the pancreas was significantly heavier in male Hcrt deficient mice compared to male WT mice. There were no changes in the size of any of the other internal organs studied here.
Conclusion: We conclude that aged male mice lacking the hypocretin peptide have decreased insulin sensitivity. Hence, they require higher insulin levels to maintain normal fasting glucose levels. 
I do not think he used female mice.  Nonetheless- very nice.  Confirmation that sugar and insulin metabolism is messed up.

I really like this study, too.  
0720  Clarithromycin for the treatment of hypersomnia: a randomized, double-blind, placebo-controlled, crossover trial
Introduction: Recent work has demonstrated that cerebrospinal fluid (CSF) of patients with primary hypersomnias enhances activity at the GABA-A receptor, and this may be causal to hypersomnia symptoms. Oral GABA-A receptor antagonists, such as the macrolide antibiotic clarithromycin, may therefore be effective hypersomnia treatment.
Results: Twenty subjects (15 women) completed the trial and were included in analyses, with mean age 33.0 years. Two subjects dropped out due to side effects. Diagnoses included idiopathic hypersomnia (n = 11), narcolepsy without cataplexy (n = 4), and hypersomnia with long sleep but normal MSLT (n = 5). Median reaction times on the PVT (primary outcome) were not different with clarithromycin. In contrast, significant improvements with clarithromycin were seen for Epworth at week two. Differences between clarithromycin and the baseline and placebo conditions were confirmed with pairwise tests. 
Conclusion: In this pilot study, clarithromycin improved subjective sleepiness in GABA-related hypersomnia. Larger trials of longer duration are warranted
Although the authors chose it because of its effect on GABA, Clarithromycin has a couple other properties that are way more interesting to me.
  • It is an antibiotic.   It is used to treat pharyngitis, tonsillitis, acute maxillary sinusitis, bronchitis, pneumonia, periodontitis and skin infections.   Uh huh.
  • It also affects sugar-insulin metabolism. Careful monitoring of glucose is recommended.  The inhibition of CYP3A enzyme by clarithromycin may cause hypolgycemia when used concurrently with insulin.   That may be how it affects the GABA response.  
Okay, that's all for now.   I have a doc started with the other abstracts I found interesting,  will try to finish it up and add it on here in a little while.