This study was pretty interesting.
Three groups of women:
1) normal weight
2) gynoid obesity (stores more fat in hips & butt), defined by WC/HC < 0.85
3) android obesity (stores more fat in belly, which is rare in women), defined by WC/HC > 0.85
First, we get confirmation that insulin sensitivity (IS) is better in morning than evening. But then we get these interesting glucose tolerance curves:
Fat stored in your hips & butt is thought to be healthier than that stored in your belly region. This is confirmed here. Gynoid obesity, while exhibiting an attenuated AM/PM difference, was able to restore euglycemia by the end of the experiment at both time points. Ie, gynoid obesity selectively improved IS in the evening.
Android obesity, which is more nefarious than gynoid (also confirmed here), had a similar though not as robust effect in the evening but deteriorated IS in the morning.
One potential interpretation: it’s better to have a little extra fat stored in your hips and butt than to be lean or have belly fat. However, I have a qualm with that interpretation. Healthy people show a robust circadian difference in glucose tolerance. Just as insulin resistance (IR) is an accepted physiological phenomenon observed in some ketogenic dieters, I view this circadian difference, also, as physiological.
Part 2. Part of the mechanism appears to be mediated by the beta cells via insulin secretion. In normal weight, beta cells secrete way more insulin in the evening to try and overcome IR, but fail, resulting in glucose intolerance. It’s essentially “insulin hyposecretion” in the evening, bc even though insulin secretion is higher than in morning, it’s not enough to restore euglycemia (bc “physiological circadian IR” in the evening).
Gynoid obesity (the “good” kind) secretes just enough insulin to match IS, keeping blood glucose normal. This appears to be a true reflection of blunted circadian variation in IS.
Lastly, android obesity secretes more insulin in the morning, which keeps glucose under control, but less at night suggesting some of their PM IR is actually beta cell failure. Sort of.
Tl;dr: Normal weight IR at night is more due to glucose intolerance at the level of skeletal muscle (and/or possibly liver). The authors even refer to the normal weight IR in the evening as “physiological IR,” because we’re supposed to be burning fat at night. I concur.
Android obesity glucose intolerance at night is at least partly due to beta cell failure. Sort of.
Gynoid obesity reflects a sort of “physiological hyperinsulinemia,” which basically means it’s enough to restore euglycemia but not induce hypoglycemia. In other words, it’s not that bad because it matches IS; if the normal weight beta cells could do this in the evening, they wouldn’t be hyperglycemic.
More insulin would be healthier in this #context, unless like me, you believe circadian variations are physiological and normal because we are humans who live on Earth.
Android obesity (the rare kind) can be said to exhibit “selectively bollixed compensatory hyperinsulinemia.” Ie, they appear to be IR in the morning, but not hyperglycemic bc high insulin secretion, but glucose intolerant at night bc they’re still IR, but don’t have enough insulin to overcome it. Circadian rhythms of glucose tolerance appear to be attenuated in this subgroup of obesity, both at the level of skeletal muscle (and/or possibly liver) and the beta cell, depending on the time of day. Sort of.
Lastly, I do not think there is a linear progression from normal weight to gynoid obesity to android obesity. But rather, it seems more plausible that: 1) “normal weight -> circadian fail X -> android obesity;” and 2) “normal weight -> circadian fail Y -> gynoid obesity -> pseudo-protective adaptation.” Maybe, but either path will result in diabetes if the underlying cause isn’t addressed.
What is this “pseudo-protective adaptation?”
I don’t know.
Food for thought.