I only asked bc before the advent of recombinant Insulin (AKA HUMALIN) lipodystrophy was MUCH more common. The MOA was thought to be immune mediated, or an "allergy" of sorts to the insulin being used at the time, which was derived from an mammalian concentrate usually SWINE.
Current evidence supports the yesteryears theory as the frequency dropped remarkably once recombinant Insulin was introduced. That being said injection related lipodystrophy (there are several types and categories) still occurs is DM patients and the most likely explanation is altered focal cellular metabolism, or more specifically the catabolism of Triglycerides into fatty acids and glycerol.
(Yea I know that doesn't follow physiologically as Insulin generally enhances lipogenesis. However bear in mind diabetics exhibit varying degrees of glucose intolerance, that is further complicated by suppressed insulin sensitivity. Thus counter regulatory hormones such as GH and Cortisol could/would also be contributing factors )
I found it interesting, if not perhaps contradictory, SKM ATROPHY was also observed as a contributing factor in some DIABETIC PATIENTS with lipodystrophy.
Regardless lipodystrophy has also been reported with chronic rHGH use and the MOA is also thought to be due altered focal cellular metabolism.
The recommended treatment
- Rotate the injection sites
- Limit the amount of GH pinned in each site
- The absolute amount varies as few patients develop lipodystrophy from GH use IME
but I suppose TWO IU or less would be a reasonable staring point
jim
