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I think the problem here is that the carbs can "overflow" the fat storage cells while protein or fat cannot do this. Or perhaps we can ingest unlimited amounts of carbs while too much protein or fat would make us sick. The fat cells bursting from overload are then the irritant which starts the inflammatory cascade. Other unrelated irritants are e.g. AGEs/ALEs or uric acid crystals. I came to the conclusion that sugar consumption is safe as far as the fat storage cells (adipocytes) are not completely filled with the storage fat. This is my post I also made on the other group:
It has become apparent that the evolution did not think wisely about
the design after the reproductive age is over so that our aging just
represents the developmental program run abruptly overtime. Another miss is that the evolution has not predicted that we may ever run into carbohydrate overfeeding lasting longer than a few weeks in the summer. In the early forming days carbohydrates were scarce and present mostly in root vegetables. Thus the evolution made every effort to make energy reserves from them (e.g. giving us multiple copies of the amylase genes) not bothering to create a regulatory mechanism to stop "filling the tanks" when they are full (because they apparently never got full). The novaday lifestyle represents continuous carbohydrate excess combined with sedentary lifestyle so the tanks are always being filled and "never" taken from unless people live physically active lifestyle. The "tanks" are called adipocytes and when they cannot take more volume of fuel (fat) which is being pushed into them by the "harsh biochemical forces" they just burst open. This is of course sensed by the body as a damage and an inflammatory repair response is mounted. Because the feeding and adipocyte bursting keep going on the inflammatory response never has chance to finish its job and is struck in the original "destructive" phase resulting in the well known chronic systemic inflammation. Following are some citations describing the inflammatory response against the irritant (bursting adipocytes overloaded with fat made from sugar). If we could develop a sensor telling how much fuel we have in our tanks we could prevent many of the chronic diseases of today. At least the evolution gave us the brains so that we can construct one. Unfortunately, the medical establishment is rather interested in suppressing the consequences with inhibitors of the inflammatory response like NSAIDS rather than making such sensor. And
the food industry keeps feeding us the cheap carbs in excess as well as providing other nutrient/mineral depleted food which makes us hungry even more ...
Taka
P.S.: Of course it's not as simple as this as there are other factors
in play such as PUFAs inhibiting the basal metabolism (via thyroid)
which can burn some of the extra carbs before they are put into the
storage.
J Clin Invest. 2007 Jan;117(1):175-84.
Obesity induces a phenotypic switch in adipose tissue macrophage
polarization.
Lumeng CN, Bodzin JL, Saltiel AR.
Life Sciences Institute, University of Michigan, Ann Arbor, Michigan
48109, USA.
Adipose tissue macrophages (ATMs) infiltrate adipose tissue during
obesity and contribute to insulin resistance. We hypothesized that
macrophages migrating to adipose tissue upon high-fat feeding may
differ from those that reside there under normal diet conditions. To
this end, we found a novel F4/80(+)CD11c(+) population of ATMs in
adipose tissue of obese mice that was not seen in lean mice. ATMs from
lean mice expressed many genes characteristic of M2 or "alternatively
activated" macrophages, including Ym1, arginase 1, and Il10. Diet-
induced obesity decreased expression of these genes in ATMs while
increasing expression of genes such as those encoding TNF-alpha and
iNOS that are characteristic of M1 or "classically activated"
macrophages. Interestingly, ATMs from obese C-C motif chemokine
receptor 2-KO (Ccr2-KO) mice express M2 markers at levels similar to
those from lean mice. The antiinflammatory cytokine IL-10, which was
overexpressed in ATMs from lean mice, protected adipocytes from TNF-
alpha-induced insulin resistance. Thus, diet-induced obesity leads to
a shift in the activation state of ATMs from an M2-polarized state in
lean animals that may protect adipocytes from inflammation to an M1
proinflammatory state that contributes to insulin resistance.
PMID: 17200717
J Lipid Res. 2005 Nov;46(11):2347-55. Epub 2005 Sep 8.
Adipocyte death defines macrophage localization and function in
adipose tissue of obese mice and humans.
Cinti S, Mitchell G, Barbatelli G, Murano I, Ceresi E, Faloia E, Wang
S, Fortier M, Greenberg AS, Obin MS.
Institute of Normal Human Morphology, University of Ancona, Ancona,
Italy.
Macrophage infiltration of white adipose tissue (WAT) is implicated in
the metabolic complications of obesity. The precipitating event(s) and
function(s) of macrophage infiltration into WAT are unknown. We
demonstrate that >90% of all macrophages in WAT of obese mice and
humans are localized to dead adipocytes, where they fuse to form
syncytia that sequester and scavenge the residual "free" adipocyte
lipid droplet and ultimately form multinucleate giant cells, a
hallmark of chronic inflammation. Adipocyte death increases in obese
(db/db) mice (30-fold) and humans and exhibits ultrastructural
features of necrosis (but not apoptosis). These observations identify
necrotic-like adipocyte death as a pathologic hallmark of obesity and
suggest that scavenging of adipocyte debris is an important function
of WAT macrophages in obese individuals. The frequency of adipocyte
death is positively correlated with increased adipocyte size in obese
mice and humans and in hormone-sensitive lipase-deficient (HSL-/-)
mice, a model of adipocyte hypertrophy without increased adipose mass.
WAT of HSL-/- mice exhibited a 15-fold increase in necrotic-like
adipocyte death and formation of macrophage syncytia, coincident with
increased tumor necrosis factor-alpha gene expression. These results
provide a novel framework for understanding macrophage recruitment,
function, and persistence in WAT of obese individuals.
PMID: 16150820 |
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