Acarbose with food extends mice lifespan, does Acarbose "without" food also extend mice lifespan?

Acarbose has very low bioavailability, less than 2% gets absorbed as the active drug, and 35% as metabolites, it’s believed that Acarbose extends lifespan by slowing glucose absorption.

But many diabetic drugs can also slow glucose absorption, but they can’t extend lifespan much like Acarbose.
I wonder beside the reduction of postprandial glucose blood concentrations, does Acarbose extend lifespan by other pathways? such as altering the microbiome on GI tract?

I am curious if we treat Acarbose on the fasting mice, can it also has anti-aging effect?
If taking Acarbose on the fasting can also extend lifespan, then it’s a good news that we can take mega dose of Acarbose on the fasting, while avoiding those annoying adverse effects.


Acarbose acts locally in the gastrointestinal (GI) tract with low systemic bioavailability (less than 2% gets absorbed as the active drug, and 35% as metabolites).


Good question… what is the overlap with caloric restriction? It hasn’t been tested, but it would be interesting to find out.

But ultimately maybe the better question is how well it works with other longevity medications because real Caloric Restriction with Optimal Nutrition (reducing caloric intake by 30% to 50% over many years while still getting all the important nutrients that your body needs) is so hard, and so unpleasant (I’ve tried it for a year) that I think the percent of people who could do it and would continue to do it for years, is likely under 1% of people, so its kind of irrelevant.

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This is a great question because I do very low carb most days and I have the same quandary. Can they put mice on a keto diet? Do they ever?

The confusion arises because acarbose is an mTOR inhibitor, so it may be extending lifespan purely due to that pathway and nothing to do with glycemic control.

There’s also confusion around the SGLT’s because it’s very possible that they act via a klotho pathway, and again, nothing to do with glucose control.

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The more simple explanation sounds more plausible in my opinion. Glucose and insulin are both inflammatory. It seems to me that much about mammalian health links to glucose. The leading causes of death are strongly linked to glucose and the mechanism of so many known ways to improve health do so as well: caloric restriction, time restricted feeding, metformin, exercise, ketogenic diet, etc. What would be different about acarbose mechanism of action? I’m personally doubtful about the benefits of acarbose without food.

citation needed for it being an mTOR inhibitor

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ACA exposure also reduces mTOR signaling in liver and kidney tissues [2, 8]. 17aE2 is a non-feminizing steroid that has a reduced affinity for the classical estrogen receptors

Source: Rapamycin, Acarbose and 17α-estradiol share common mechanisms regulating the MAPK pathways involved in intracellular signaling and inflammation | Immunity & Ageing | Full Text

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Miglitol - Wikipedia gets absorbed - we urgently need ITP on this. Why can’t we just do lower-sample size and much denser analytics?

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Could this be possibly downstream from blunting glucose spikes?

The multiple morbidities are actually secondary to diabetes rather than glucose per se . If it were strictly glucose then very strict glycemic control of diabetics would greatly lower end organ damage and mortality rates. Very major studies have shown that that is actually not the case.