Metformin for insulin resistance

I currently have an insulin pump but have insulin resistance. The more reading I'm doing online, the more I'm learning. I'll be able to see an endocrinologist (for the first time) soon and I'm making a list of things I want to discuss while I'm there. My insulin resistance is certainly one of them!

I'm seeing that some people take Metformin to help with insulin resistance, along with insulin/pump therapy. Do any of you do this or have any experience with this?

When I was on only Metformin, it didn't really help me. After some research I now see my primary care doctor did not have me on enough and never increased the dose in the way she should have to see a more desirable result. Does anyone have any experience with how the dosing is typically done. Do people normally start out on 500mg and then go up from there? When I was on it I did experience GI issues. If I ever used it again, this is something I would want to be careful of. I've been told the dose is increased in order to ease some of those GI issue during the transitional period. I know everyone is different but it would be nice to have a general idea.

Sorry so many questions. The more knowledge I gain, the more I want. :)

My experience is different than most but have used metformin for last 12 years.

Yes I am type 2 but frankly all the data I have is that Metformin reduces excess liver glucose release during fasting.

IT was originally specified to reduce insulin resistance. On this score I am not impressed.

Generally as I understood it, doses were started at 500 mg and increased as deemed necessary by your Doctor/Endo.

My experience today suggests that if your liver has faulty signalling reading the insulin of blood stream during fasting causing excess glucose release, the metformin will reduce that and reduce insulin consumption.

I am not in mainstream on this but my take on insulin resistance is due to body pushback from excess glucose loading up temporary glucose storage space of skeletal muscles and fat cells.

One of the theories on metformin is that it reduces insulin resistance in the cells helping cells store more glucose on insulin in bloodstream command.

Latest findings on metformin operation ( not theories/guesses of operation) are :
Science News
... from universities, journals, and other research organizations
Most-Used Diabetes Drug Works in Different Way Than Previously Thought
Jan. 6, 2013 — A team, led by senior author Morris J. Birnbaum, MD, PhD, the Willard and Rhoda Ware Professor of Medicine, with the Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, found that the diabetes drug metformin works in a different way than previously understood. Their research in mice found that metformin suppresses the liver hormone glucagon's ability to generate an important signaling molecule, pointing to new drug targets. The findings were published online this week in Nature.
For fifty years, one of the few classes of therapeutics effective in reducing the overactive glucose production associated with diabetes has been the biguanides, which includes metformin, the most frequently prescribed drug for type 2 diabetes. The inability of insulin to keep liver glucose output in check is a major factor in the high blood sugar of type 2 diabetes and other diseases of insulin resistance.
"Overall, metformin lowers blood glucose by decreasing liver production of glucose," says Birnbaum. "But we didn't really know how the drug accomplished that."
Imperfectly Understood
Despite metformin's success, its mechanism of action remained imperfectly understood. About a decade ago, researchers suggested that metformin reduces glucose synthesis by activating the enzyme AMPK. But this understanding was challenged by genetic experiments in 2010 by collaborators on the present Nature study. Coauthors Marc Foretz and Benoit Viollet from Inserm, CNRS, and Université Paris Descartes, Paris, found that the livers of mice without AMPK still responded to metformin, indicating that blood glucose levels were being controlled outside of the AMPK pathway.
Taking another look at how glucose is regulated normally, the team knew that when there is no food intake and glucose decreases, glucagon is secreted from the pancreas to signal the liver to produce glucose. They then asked if metformin works by stopping the glucagon cascade.
The Nature study describes a novel mechanism by which metformin antagonizes the action of glucagon, thus reducing fasting glucose levels. The team showed that metformin leads to the accumulation of AMP in mice, which inhibits an enzyme called adenylate cyclase, thereby reducing levels of cyclic AMP and protein kinase activity, eventually blocking glucagon-dependent glucose output from liver cells.
From this new understanding of metformin's action, Birnbaum and colleagues surmise that adenylate cyclase could be a new drug target by mimicking the way in which it is inhibited by metformin. This strategy would bypass metformin's affect on a cell's mitochondria to make energy, and possibility avoid the adverse side effects experienced by many people who take metformin, perhaps even working for those patients resistant to metformin.

Each of us responds differently, of course . . . but my experience parallels Jim's. I've been on Metformin for a few years now and I don't see it having much effect on insulin resistance. For me, the real benefit is simply to retard liver dumping, as described above.

I also needed to add for me that minimum the dosage that hauls back liver seems to be from 500 mg to about 700mg and lasts as long as met is up to strength in blood. ( 2.5 hours up to strength after ingestion, 1 to 3 hours at strength and 1/2 to 1 hour being swept out by kidneys)

250 useless and some generic brands cannot put out enough met (although rated 500mg)

So much fun.

Thanks so much for this information!Great!

Thanks for the reply, DNS!

I find metformin a big help with insulin resistance. I started it a few months ago and in that time, I've been able to lower my basal by about 25%. I need somewhat less mealtime insulin, too. Unfortunately, it hasn't helped as much with dawn phenomenon as I would like, but maybe I need a higher dose.

I'm grateful that I have no GI issues with metformin. I've read that the extended release version of the brand name, Glucophage, is less likely to cause GI issues. Due to my insurance, I take the regular old generic, and started with 500mg and gradually went up to 1000mg. Good luck, if you decide to try it again!

What times are you taking metformin for dawn ph?

For me; I take a dose at 10:00pm and a dose at 12:00am midnight and this seems to stop dawn phen for me while the two doses appear to cover from 12:30 am throught to 5:00/5:30 am. A single large dose was useless and did no good.

As I am not Doctor, I can not recommend for you and do not know if that helps?

Prior to this my dawn Ph would be 238 in am. Also prior to met doses,my dawn ph would start agressively releasing glucose at 3:00 am and be 150 and increase to 238 by 6:00 am

best wishes and good luck.