-1
$\begingroup$

Considering that the sequestering of 'persistent organic pollutants' [POPs] by adipose tissue is now established (see Toxicological Function of Adipose Tissue: Focus on Persistent Organic Pollutants by La Merrill et al. Environmental Health Perspectives, 121, 2013, pp162-169; pdf available here), is there any evidence that the existence of such POPs within fat cells interferes with the function of leptin, in particularly with the normal suppression of appetite in the hypothalamus?

Were there in fact such evidence, could such a derangement in leptin function account for tendencies to obesity in populations exposed to POPs?

$\endgroup$
  • $\begingroup$ The normal function of adipose tissue is to stare triglycerides. Please quote a source for your statement about organic pollutants (and for goodness sake don't abbreviate them as POPs). $\endgroup$ – David Apr 29 '18 at 17:54
  • $\begingroup$ It seems fairly well accepted that part of the function of AT is to store fat soluble toxins such as OPs. [e.g. Env.Health Perspectives 121(2) La Merrill]. There is a Korean study citing numerous references and discussing the relation of OPs to obesity [Obesity Reviews 18(2) Y-M Lee]. However, I could find no study which proposes an underlying mechanism according to which, presuming that the accumulation of fat serves an entirely necessary--rather than erroneous--function in all cases, dysfunction in the leptin-mediated circuit induced by OPs in AT is implicated. If so, it would explain a lot. $\endgroup$ – jeremiah May 1 '18 at 9:16
  • 4
    $\begingroup$ How do you differentiate between "function" and "they happen to accumulate there because they are fat-soluble? I thought it was the P450 system that had the function of dealing with toxic compounds, the endpoint being elimination (not sequestering). Whatever the connection between modern organic pollutants and obesity, you should remove the assertion that the normal function of adipose tissue is to sequester these compounds. $\endgroup$ – David May 1 '18 at 10:17
  • $\begingroup$ Perhaps it is more pertinent to ask to what extent fat cells discriminate between lipophilic organic compounds; the point being that because in the general case they do not, it is not unreasonable to argue--without quibbling over semantics or even raising the philosophical issue of intention--that this capacity for AT to dissolve, thus temporarily sequester organic pollutants within the process of their eventual detoxification--if this is indeed possible--, therefore protecting vital organs from the harmful action of these compounds. I will elaborate a little in answer to the question. $\endgroup$ – jeremiah May 4 '18 at 8:03
  • $\begingroup$ @user1136 That is good editing, and resolves some of the earlier objections to the question. I don't think my own answer which was effectively prompted by those unfounded objections in order to clarify that question deserves its down-votes by the way; since in the main what it states is correct, while contention about its latter paragraphs--which need not have been included but were-- is essentially a matter of opinion. $\endgroup$ – jeremiah Aug 5 at 15:48
2
$\begingroup$

Leptin is the satiety hormone produced in the body fat cells - increased blood leptin levels suppress appetite and decreased levels stimulate it.

Persistent Organic Pollutants (POPs) are man-made chemicals that are environmentally persistent, leading to bioaccumulation in the food chain. Examples include polychlorinated biphenyls (PCBs) and polybrominated diphenylethers (PBDEs).

In the only study I've found that mentions the direct relationship between POPs and blood leptin levels, the exposure to POPs was associated with decreased leptin levels in women but not men: Expression of Obesity Markers and Persistent Organic Pollutants Levels in Adipose Tissue of Obese Patients: Reinforcing the Obesogen Hypothesis? (PlosOne, 2014):

Our study revealed a negative association between leptin serum concentrations in women, and the levels of several PCBs and BDE153 in both fat depots. Remarkably, in men, none of the analysed POPs correlated with leptin serum concentration.

In another study, the exposure POPs was associated with decreased levels of leptin in breast milk: Association between Several Persistent Organic Pollutants in Serum and Adipokine Levels in Breast Milk among Lactating Women of Korea (Environmental Science and Technology, 2015):

Leptin concentrations in breast milk were negatively associated with ∑hexachlorohexane (HCH), oxychlordane, ∑chlordane, or 2,2',4,4',5,5'-hexachlorobiphenyl (CB 153) levels in maternal serum.

Both studies suggest, directly or indirectly, that persistent organic pollutants can decrease leptin levels and thus stimulate hunger, but the studies were small and are not, at least for me, considered sufficient evidence.

$\endgroup$
  • $\begingroup$ Excellent work.You understand the question, the possible importance of its consideration and have given a good informative answer. I agree that there is little evidence of the association, but continue to believe that it deserves more investigation. Naturally it would be difficult to establish a direct relation between POPs sequestered in fat cells and leptin function deriving in those cells; first it would be interesting to find if POPs are in fact present in fat cells of the obese. As you see, someone is so offended by my answer that he repeatedly down-votes it without proper reason. $\endgroup$ – jeremiah Aug 5 at 13:00
  • $\begingroup$ @jeremiah, leptin is present in the fat cells of lean and obese people. I'm not sure how much the leptin levels fluctuate within the fat cells and if this has any importance, but it's the leptin that is released into the circulation that affects appetite in the hypothalamus. $\endgroup$ – Jan Aug 5 at 13:13
  • $\begingroup$ @Jan.I know that leptin is produced in fats cells; the point of the question is whether the presence of POPs in the fat cells of obese people interferes with the conformation of leptin rendering it less effective at the H/T or even inert. The first question is to ascertain whether POPs are present in greater degrees in the fat cells of the obese than in a control group; and if not, whether they nevertheless exert a deleterious effect on leptin synthesis. If the leptin isn't working, then that's 'leptin resistance' isn't it. You're a young researcher aren't you? Well, there you are. $\endgroup$ – jeremiah Aug 5 at 13:26
  • 1
    $\begingroup$ @jeremiah, from what I understand from the linked studies, the higher amount of POPs in the fat cells is associated with lower levels of leptin in the blood. I assume this is due to decreased release of leptin from the fat cells into the circulation. I have no idea if POPs affect leptin when there are still in the cells. $\endgroup$ – Jan Aug 5 at 13:34
  • $\begingroup$ That's a start; and it may end up being the principal effect. I haven't yet read the linked articles; but I'll get to it. Thanks by the way for your effort in uncovering them. One of the reasons this is important is to establish some cause for leptin resistance which is associated with obesity; not necessarily so that it may be redressed, but at least that obesity might be better understood as a condition of 'leptin resistance', rather than a syndrome of grievous gluttony and sloth as it is often portrayed. $\endgroup$ – jeremiah Aug 5 at 13:48
-3
$\begingroup$

It seems that the answer to this question is at present no--and might remain so until or unless researchers dedicated to elucidating any such relation between leptin and obesity are prepared to subject some population of poor leptin-producing creatures to given organic pollutants, with the aim of determining any measurable effect on leptin capability--a difficult assignment to say the least.

Various studies seeking to confirm the so-called 'obesogen hypothesis' have not unreasonably argued a mechanism of 'endocrine disruption' by certain common organic pollutants, but these are neither comprehensive nor capable of resolving certain paradoxes in the relation between leptin and obesity: notably that leptin levels are routinely observed to be raised in cases of severe obesity. The idea of some derangement in leptin function induced by a local cause therefore becomes attractive in explaining such 'leptin resistance'.

At the same time, it is probably negligent to blame rising levels of obesity merely upon the delinquent appetites and profligacy of affluent people, particularly when certain benefits of fat accumulation, apart from the sheer simple joy of being fed, have been observed: putatively there are diminished rates of neuro-degenerative disorders such as Alzheimer's disease in the mildly obese. (There are various studies drawing such conclusions). Possibly such effects also pertain to the capacity for adipose tissue (AT) to sequester organic pollutants.

Now the respondent to this question has objected to the characterisation of this latter effect as a 'function' of AT when it is clear that this capacity for fat cells to accommodate fat-soluble substances without the necessity for their elaborate discrimination is indeed inherently and innately part of the broader function of AT. The inference of the question itself is in fact that the proliferation of fat cells and fat mass in obese individuals may serve precisely this purpose or function.

Such an assertion requires no troublesome incursion into philosophical or teleological dispute--regarding ultimate cause or intention--nor great excesses of the imagination--that for example we are essentially organic creatures increasingly immersed in the products of oil and other hydrocarbons, themselves loosed from the ancient abeyance of that essential nature--, only the understanding that part of the actual mundane function of fat stores is to hold in continuing abeyance those organic compounds, in particular those which are broadly derivatives of hydrocarbons, which the organism generally is unable either to accommodate elsewhere in its metabolism, as if effectively indigestible food, or successfully to excrete.

It might be emphasised here that the aim of any such inquiry into the relation between organic pollutants and obesity--possibly mediated by a derangement in leptin function--is not of itself to redress any such local cause determined empirically; since realistically such would come only with the inevitable obsolescence of oil and the derivatives of hydrocarbons generally: petroleum, plastics, organic pollutants etc.

The aim is to elucidate the nature of this phenomenon of modern obesity, that at least it might be understood as part of universal necessity, that indeed it must in principle serve some eventual 'evolutionary advantage', not of a family of reproducing organisms--although this is an aspect of it--, but of the universal entirety itself in eternity (which some are emboldened by a peculiar philosophical perspective of the absolute inviolability of such a universal unity to characterise as the 'Unitary Soul', for want of a better description of the singular dynamic and process which must enliven it).

I might add here that there has developed an obsession in the biological sciences with a theory of evolution based not only on the philosophically repugnant idea of 'chance'--which despite the fervour with which such a paradigm is defended cannot of course be quantified in any meaningful way; which incapacity of itself requires that the entire notion be removed from orthodox thinking--, but on the necessity to impute to some detail of formal biological reality an evolutionary advantage conferred by such happenstance (e.g. in the usual view, base mutations) within some limited context, the niche, of which it is in any event merely an aspect, when the ultimate parameters of such advantage, more especially in the greater spatial and temporal context are essentially unknowable.

This is not to dispute the absolute preeminence of an 'evolutionary principle' within universal reality; only to argue that this principle is entirely singular and simply inherent within the fact of existence itself; and most importantly that the ultimate parameters of such a principle can never be objectively discriminated or 'known' by those such as we mere humans entirely immersed within the mechanics of an inviolate universal unity in eternity. No conception of an ultimate 'evolutionary disadvantage' may be formed without the possibility for knowledge of the ultimate intention of such a dynamic universal unity.

And for those who would object that such an 'a priori' postulate of universal unity is improperly metaphysical in character, it would be well for them to remember that the existing scientific and cultural ethos of a blind aimless nature--Dawkinsism--, and the preeminence of 'happenstance' as its primary impetus--which is to say the denial of singular universal cause and intention merely for want of the capacity to discern it--, is only the expression of a passing alternative school of philosophy and its guiding paradigm, essentially that of 'chaotic erroneous nature' groping its cruel meaningless way aimlessly in the eternal darkness awaiting only the guiding hand of Man to render 'order' within it.

$\endgroup$
  • 1
    $\begingroup$ IMO you need to quote sources. here is one, maybe. Although the accumulation of POPs by adipose tissue is now beyond dispute (and very disturbing) [ref 1 of the cited ref], the hypothesis that this contributes to obesity is surely unproven, and may or may not involve leptin? $\endgroup$ – user1136 Aug 4 at 13:45
  • 1
    $\begingroup$ This answer is frankly terrible and one of the worst ones I have seen on this site. I would normally recommend adding references but I don't think even that can save it from all the illogical tangents and wrong statements. Universal unity? Unitary soul? A complete lack of any understanding of evolution? $\endgroup$ – Bryan Krause Aug 4 at 16:41
  • 1
    $\begingroup$ @user1136. The reason for the post was to ascertain whether this was an original idea; since my suspicion is that it seems too obvious a connection not to have been conceived and studied previously; there were no references which I could find. As such, the reference from a 2014 paper demonstrates that it is neither a novel idea nor without foundation, in spite of the previous reception of the question here. Moreover, there would seem considerable potential to investigate the idea that it is such a derangement in leptin metabolism which is at the root of obesity, if only to understand it. $\endgroup$ – jeremiah Aug 5 at 8:50
  • $\begingroup$ Of course the hypothesis is unproven, nor have I supposed or stated otherwise; but I believe that part of the purpose of forums such as this is to air such ideas among those with the where withal and inclination to pursue them. That latter part of my answer is intended only to express a particular philosophical perspective--just a form of old-fashioned determinism really, newly expressed--, the implication of which is that whatever mechanism is finally established for the effect that in the modern day, there are some who simply cannot satisfy their appetites, it is nonetheless an entirely.. $\endgroup$ – jeremiah Aug 5 at 8:56
  • 1
    $\begingroup$ @Bryan Krause. With respect, sometimes an answer requires a different philosophical perspective, particularly when the principal foundation of the traditional answer is merely a prevailing philosophical view. At the same time, it is not my intention here to expatiate thus.In this case, a good well considered question was asked and because it was roundly derided, I answered it myself in the hope of elucidating the idea. As you now see, there is good evidence that the idea has merit. I do wish therefore that you would please not continue to attack this and other questions; rather answer them. $\endgroup$ – jeremiah Aug 5 at 13:18

Your Answer

By clicking “Post Your Answer”, you agree to our terms of service, privacy policy and cookie policy

Not the answer you're looking for? Browse other questions tagged or ask your own question.