Evidence for competing effects of body mass, hyperinsulinemia, insulin resistance, and androgens on leptin levels among lean, overweight, and obese women with polycystic ovary syndrome.
Remsberg KE, Talbott EO, Zborowski JV, Evans RW, McHugh-Pemu K.
Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pennsylvania 15261, USA.
OBJECTIVE: To evaluate the relationships between leptin, body composition, insulin resistance, androgens, and reproductive indices among women with polycystic ovary syndrome (PCOS).
CONCLUSION(S):Below a certain BMI, hyperandrogenic women with PCOS have lower leptin levels than controls. Conversely, overweight and obese PCOS subjects appear to produce insufficient leptin for a given fat mass, relative to the degree of hyperinsulinemia, potentially because of the competing effects of adipocyte insulin resistance and androgens on leptin.
DESIGN: Matched case-control study.
SETTING: Academic reproductive endocrine practice; school of public health.
PATIENT(S): Forty-six Caucasian women with PCOS and 46 population-based controls matched by age and body mass index (BMI).
INTERVENTION(S): None.
MAIN OUTCOME MEASURE(S): Leptin, insulin, androgenic hormones, body composition parameters; reproductive parameters.
RESULT(S): Overall, leptin levels among women with PCOS did not differ significantly from those of control women (20.4 +/- 14.9 vs. 21.9 +/- 14.3 ng/mL). However, within the lowest BMI tertile, women with PCOS had significantly lower leptin levels (9.6 vs. 18.3 ng/mL), comparable insulin, and higher testosterone concentrations than controls of similar body mass. Within the overweight and obese subgroups, both insulin and testosterone levels were increased among women with PCOS; leptin levels, although higher among obese cases, were not statistically different than those in controls.
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Hey, SoulCysters! Need to eat more veggies, but can't find recipes??
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So since I dont really understand leptin I did some research on it. From what I read when a person consumes more calories then burnt and it turns to fat the adipose tissue will release more leptin so the person will eat less and vice versa. I also read that a reason for low leptin is due to sleep deprivation which will cause you to be more hungry in return.
So is it that simple? Are us thin cysters not getting enough sleep?
Bump b/c I've been doing some research on leptin and do not quite understand this. So for thin cysters, they may not be producing enough leptin for body weight? I'm nos sure I get this.
so our insulin levels are more or less the same as 'normal' women, its just the testosterone that is higher - and this has something to do with Leptin. Is that correct?
Okay, so now I'm REALLY confused. If our insulin levels are just like "normal" women without pcos, then why do we take metformin, and watch our diet? I always thought most thin women's pcos was in some way still connected with insulin, even if the connection is less apparent than overweight pcosers. Can someone clear this up for me? Thanks!
Leptin is a hormone that is produce by the fat cells of the body - The main purposes of leptin seems to be to help regulate the amount of body fat and if everything is working properly to prevent the accumulation of too much body fat. It does this by communicating to the the brain (the hypothalamus) that the body has adequate fat/energy stores - which tells the hypothalamus to reduce the appetite for food and possibly raises the metabolism. The word Leptin is derived from the Greek word for "thin". Basically more Leptin (or more sensitivity to Leptin) leads to thinness.
Leptin is probably one of the more important substances in our bodies for determining things like appetite, metabolic rate and body fat/body weight.
The vast majority of of overweight/obese people are resistant to Leptin.
The Book "Mastering Leptin" seems to assert that Leptin resistance is positively correlated with Insulin Resistance.
CONCLUSION(S):Below a certain BMI, hyperandrogenic women with PCOS have lower leptin levels than controls.
Perhaps "thin cyster" are unusually sensitive to the effects of leptin???
Perhaps I am wrong but I think that often thin cyters still have some degree of insulin resistance -- (maybe someone could verify the fact on that one for me) -- if that were true it would seem to someone contradict the assertion that Leptin resistance is positively correlated with Insulin Resistance -- although I think that with PCOS and a lot of this stuff exceptions and indivdual differences are pretty common.
Quote:
Conversely, overweight and obese PCOS subjects appear to produce insufficient leptin for a given fat mass, relative to the degree of hyperinsulinemia,
I think that generally speaking more fat mass = more leptin
I would guess that also hyperinsulinemia (more insulin) would = more leptin
. . . . .but that both more fat and more insulin would = less leptin sensitivity. . . . . (because like with insulin/insulin sensitivity) more leptin = less leptin sensitivity.
Quote:
potentially because of the competing effects of adipocyte insulin resistance and androgens on leptin.
I have not ever tried to look up the effects of "adipocyte insulin resistance" (I assume that mean insulin resistance of the fat cells or the body's fat??) or the effects of [excess] androgens on leptin, but contextually I am assuming that they mean that adipocyte insulin resistance and androgens tend to cause lower levels of leptin to be produced ---- is that the way you all read it too?? That might be an interesting thing to know more about!
Keep in mind, this isn't just about leptin and IR... or Leptin and BMI...
Quote:
Evidence for competing effects of body mass, hyperinsulinemia, insulin resistance, and androgens on leptin levels among lean, overweight, and obese women with polycystic ovary syndrome.
__________________
Hey, SoulCysters! Need to eat more veggies, but can't find recipes??
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Study: Androgens and leptin levels in Lean Cysters 
