The HOMA is calculated from the product of plasma glucose and insulin levels divided by a constant. In animal models the mean plasma glucose and insulin levels vary according to the species. Hence, few authors discouraged the use of HOMA model in animal studies.
How do i proceed with HOMA - IR estimation in animal models especially in mouse?
I recently had a manuscript accepted, and my reviewers had a concern with the HOMA-IR that we used in our sheep model. I validated that HOMA-IR for use in sheep, and that data will be published very soon in Domestic Animal Endocrinology.
Excellent, Christopher, enough HOMA -IR data sets correlated with medical conditions, in any species will establish the level that indicates the beginning of insulin resistance. Across the board, what will be found as the Insulin Resistance ratio rises, more pathology presents.
The article I mentioned is now in press, you can find it here:
http://dx.doi.org/10.1016/j.domaniend.2017.04.002
Good article Christopher, we see the same result in human females that are amino acid deficient during pregnancy. Do you have the nutritional breakdown of the feed used ad libitum?
Thank you Dr. Viana! Have you published those results?
The pellets are a corn, soyhull, wheat middling, alfalfa meal, and distiller by product combination consisting of 71.05% total digestible nutrients, 1.08 Mcal/kg of NEg, 1.64 Mcal/kg of NEm, 88.2% DM, 13.5% CP, and 4.05% fat on an as-fed basis. Our group published this ration, it can be found via the following doi:10.2527/jas.2010-3083
published those results?Not yet, Christopher, I got the lead from "From studies in rats, we have learned that prenatal amino acid deficiency produces offspring with preference for energy-dense foodstuffs and hyperphagia, along with tendencies for greater insulin resistance, glucose intolerance, adiposity and hypertension"
Bellinger, l; Lilley C; Langley-Evans SC; "Prenatal exposure to a maternal low-protein diet programmes a preference for high-fat foods in the young adult rat;Br J Nutr; Sept 2004;92(3): 513-520
Exactly what we are seeing in our Aruban community children. We are documenting the same response through data of women who have lost their gallbladder and documenting plasma amino acid deficiency. Clinically, obese children will present with mothers that have flaccid Triceps brachii [showing they have sarcopenia, muscle loss due to, mostly digestive inability to absorb and metabolize amino acids from protein] These woman present with high triglycerides from digestive fermentation
Did the "distiller by product" in your sheep feed contain any yeast? Active or not?
Was there any fecal analysis [lost nutrients] done on the different data groups?
It's good marker of IR but if you have control healthy group of animals to compare. And you should to use Fasting glucose for correct calculation. So you don't need to know IR values for different animals (common values maybe).
Perhaps reading this paper will help : A novel approach to monitor glucose metabolism using stable isotopically labelled glucose in longitudinal studies in mice.
https://www.ncbi.nlm.nih.gov/pubmed/23492513
Sorry for the delay Dr. Viana, I've been out of town for a conference. I believe that our feed does contain yeast, however I've been unable to verify the amount. I'll see what information our farm manager has and follow up. Also, we have not done any fecal analyses to determine nutrient loss. I believe this may be tough to correlate to the clinical side given our model is a ruminant.
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