It might help too, to understand that metformin works as a liver inhibitor. How does that matter, you ask. Here's my rough understanding of it (happy to be corrected):
What we take in as carbs, is only one source of energy we have to contend to. Another is that our bodies have a store of glucagon (sugar) inside muscles and the liver. It's in the liver that proteins and fats get converted into glucose. This gets stored and released in a steady stream through the day for the general tasks of functioning, as well as when "asked for" such as when exercising or getting a hormonal response from stress.
The sugar that is release from the liver, affects our blood sugar like eating sugar does. As a type 2 your internal insulin will be doing its best to allow this energy to be accessed and utilised, (thus helping stabilise BGs) to a varying degree. It could be doing a reasonable job, it could be doing a not so good job. It's a hard task as people with type 2 may be releasing a lot more internal sugar than non diabetics.
You'll know how well "the battle" is playing out from your fasting BG levels. It can also be contributing to higher post meal levels as a kind of layered effect.
That's where metformin comes in. It dampens this production of sugar in the liver, effectively cutting down the work your internal insulin has to do.
So you can see it's another approach to reducing the workload on your insulin. It is similar to, but not the same, as going low carb. There may be a stage that low carb is not enough, you need something to deal with the internal sugar releases too.
Metformin does more, too, I'll quote wikipedia:
Metformin - Wikipedia, the free encyclopedia Quote:
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In addition to suppressing hepatic glucose production, metformin increases insulin sensitivity, enhances peripheral glucose uptake, increases fatty acid oxidation,[45] and decreases absorption of glucose from the gastrointestinal tract.
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You mention your cholesterol, what about your A1c or BG results in general?
