There's too many unknowns about how Metformin works exactly to make a blanket statement like that. I've been reading a lot of research that it doesn't actually help IR, but more controls the dumping effects of the liver, which is thought to be increased in T2 diabetics. So there's a lot of different view points on it.
I've been on Metformin for a year now, and I thought it was due to insulin resistance. I finally asked at my last appt why I was on it, and I come to find out that my endo puts a lot of her LADA patients on it, because she feels whatver insulin we (honeymooners) are producing our bodies become just that much more sensitive to it. 'Making the most' of whatver is left.
I accept that metformin could be modestly helpful to many people who are not T2. It "tweaks" a lot of things, and a lot of tweaks could add up to a significant total effect. However, I have these two observations. 1. Isn't the increased liver dumping an aspect of IR? 2. Logically, making the body "more sensitive" to insulin means decreasing IR, because "insulin sensitivity" is the complement of "insulin resistance".
I found a 100% relevant article on liver dumping by a credentialed diabetes blogger. http://www.diabetesselfmanagement.com/blog/diabetes-metformin-and-your-liver/
"Metformin prevents the liver from dumping more glucose into the blood. Scientists used to think it worked by telling CRTC2 to cooperate with insulin (in other words, reducing insulin resistance.) But new studies have found that metformin actually works by bypassing CRTC2 and directly telling the liver cells to hold the sugar."
Right, the difference between reducing insulin resistance and bypassing it is logically important. This doesn't negate the facts and the logic that excess liver dumping is a result of insulin resistance.
Background understanding: "insulin resistance" occurs in the striated muscles (muscles other than smooth muscles), belly fat, and liver.