Another two-fer for the Thursday post bumps again this week. More explanation for why this set in the next bump.
Original Publish Date: 7/26/11
In the comments on a recent post on beta cell lipotoxicity, Ned Kock (of Health Correlator blog) posted a link to a post he made a while back entitled: Lipotoxicity or tired pancreas? Abnormal fat metabolism as a possible precondition for type 2 diabetes. This article deals with the concept of the "tired pancreas" in the development of diabetes. It seems that (and hopefully he corrects me if I'm wrong here) Ned and I agree that this is not a likely explanation for diabetes. Ned summarizes the progression of obesity induced T2 diabetes from Unger & Zhou, 2001. It is worth mentioning that Unger is often summarily dismissed from the "scientific discussion roundtable" by low carbers because of the unfortunately titled "Gluttony and Sloth" paper, that, even more unfortunately also included a biblical verse. Unger's hypothesis is very leptin-centric, but not at all incompatible with other lipotoxicity based theories. Basically, lipotoxicity is the result of dysfunctional adipocytes leading to excessive "spill-over" of fatty acids into circulation and accumulation in ectopic tissues. Unger & Zhou identify dysfunction in leptin secretion and/or signaling as the initiating factor in this process. One thing that doesn't quite add up for me here is that I keep finding citations indicating leptin action increases free fatty acids which would seem counterintuitive. In any case ...
Original Publish Date: 7/26/11
In the comments on a recent post on beta cell lipotoxicity, Ned Kock (of Health Correlator blog) posted a link to a post he made a while back entitled: Lipotoxicity or tired pancreas? Abnormal fat metabolism as a possible precondition for type 2 diabetes. This article deals with the concept of the "tired pancreas" in the development of diabetes. It seems that (and hopefully he corrects me if I'm wrong here) Ned and I agree that this is not a likely explanation for diabetes. Ned summarizes the progression of obesity induced T2 diabetes from Unger & Zhou, 2001. It is worth mentioning that Unger is often summarily dismissed from the "scientific discussion roundtable" by low carbers because of the unfortunately titled "Gluttony and Sloth" paper, that, even more unfortunately also included a biblical verse. Unger's hypothesis is very leptin-centric, but not at all incompatible with other lipotoxicity based theories. Basically, lipotoxicity is the result of dysfunctional adipocytes leading to excessive "spill-over" of fatty acids into circulation and accumulation in ectopic tissues. Unger & Zhou identify dysfunction in leptin secretion and/or signaling as the initiating factor in this process. One thing that doesn't quite add up for me here is that I keep finding citations indicating leptin action increases free fatty acids which would seem counterintuitive. In any case ...
