Source: Diabetes Journal (diabetes.diabetesjournals.org)
Summary: Gut microbiome related to metabolic diseases. Glucocorticoid excess in pregnancy reduce offspring brown fat. Changes in PPAR-gamma molecule improve TZD profile. Marginal benefit of oral insulin in beta cells. Metabolome high risk profile.
Gut microbiome, interlelukins and metabolic disease: Is there a link between a certain type of gut microbiome, low levels of IL-17 and IL-21, and risk for metabolic disease (insulin resistance, type 2 diabetes, dyslipidemia)? Yes! Has it got any practical implication for the next time you see a patient in your clinic? Certainly no! "Bad" microbiome could cause metabolic disease by reducing levels of IL-17 and IL-21, but it could otherwise be that low interleukins 17 and 21 affect insulin resistance by changing microbiome, or else it could be unhealthy diet that changes microbiome and so increase metabolic risk, being IL in this case just innocent witnesses. Could changes in microbiome affect metabolic diseases? We don't know. So, for the time being, relax and wait for the next episodes of this movie.
Late pregnancy glucocorticoid excess and brown fat. If you give dexamethasone to rats in late pregnancy, their offspring will be fat, hyperglycemic and insulinresistance. That's something anyone could have guessed. But Yan-Ting Chen and colleagues also studied their brown fat and saw it was quite undeveloped, seemingly because our good friend Ppargc1a, an important promoter of brown fat development, is suppressed by DNA methylation. Bad for the poor rats.
PPAR-gamma deacetylation protects from adverse effects of TZD. It'a a shame that glytazones have so many adverse effect (edema, weight gain, fractures), because they are otherwise good insulin-sensitizers and antiatherogenic. Longhua Liu and friends saw that changing a couple of base pairs in DNA they could create mice whose PPAR-g was like deacetylated, and so TZDs work great, very anti-atherogenic and well tolerated. Wouldn't it be good if we could do the same in humans?
Oral insulin and metabolic deterioration in high risk for type 1 diabetes. I'll tell you the end of the story: oral insulin is of no use at all to prevent type 1 diabetes, that was clearly showed in DPT-1 and trialnet trials. In spite of that, Sosenko, Skyle and other didn't give up and studied from these trials those individuals with higher risk and saw that c-peptide and glucose curves 1 year after oral insulin behaved better than after placebo. That won't give them the Nobel, but they got a paper in Diabetes, not bad.
Circulating proteins and risk for type 2 diabetes. Gudmundsdottir, in exchange for an unpronounceable name for those living outside Iceland, had a powerful tool called Slow-Off rate Modified Aptamer (SOMAmer), that could detect 5034 proteins in a single serum sample, and studied if it could help us detect individuals at high risk for type 2 diabetes. He found at least 15 candidate proteins. I'll show you a picture that'll make you understand it right away:
It could be my fault if you didn't get it right. For further details please visit https://diabetes.diabetesjournals.org/
