Är antalet fettceller permanent eller ej enligt senaste rönen?

[Madness]

Har läst på mycket om detta nu ikväll, angående själva mängden fettceller, jag har förstått att om fetcellerna blir fyllda och inte räcker till kan kroppen skapa fler fettceller genom hyperplasia för att fylla behovet av fler energidepåer som då sägs vara permanenta enligt dem forskarrönen jag hittat, dvs har detta väl skett så kan inte fettcellerna försvinna, dem dör över tid men förnyas med samma mängd som dem flesta andra celler i kroppen som jag förstått.

Så denna mängd fettceller sägs bestämmas i tidig ålder, beroende på genetik, övervikt etc. Det verkar även vara så att en person med fler fettceller har svårare att hålla en låg fettprocent än en med färre fettceller då denna lättare lagrar in fett. Om denna effekt är permanent vore det trist därför att man permanent nedsätta sin möjlighet att se rippad ut genom att ha slarvat i någon period i sitt liv (grisbulk någon? :hbang:) Är inte riktigt intresserad huruvida det går att göra genom droger eller fettsugning, utan om det t.ex. är möjligt genom att gå ner i vikt o hålla sig där en längre period så att kroppen inser att den kan släppa cellerna?

Rent spontant tyckte man ju att kroppen borde vara smartare än så och kunna göra sig av med fettcellerna igen när dem inte behövs? Finns det något som bevisar att det kan vara så trots mycket som tyder på motsatsen att dem är just permanenta? Och hur stor inverkan har egentligen mängden fettceller? Finns det några fördelar för kroppen att spara på dessa fettceller även om dem förblir tomma egentligen?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC24345/
Denna studie är väl allt jag hittat som vad jag förstår tyder på att kroppen har en mekanism för att döda dessa celler? Någon kunnig som är insatt i nyaste rönen, som kan sätta lock på mina tankar för tillfället? king grub kanske:D?


"In light of the detrimental effects of obesity, it is not surprising that the body has developed numerous mechanisms to counter excess adipose accumulation. Many of these factors, including leptin and TNFα, are secreted by the adipocyte in proportion to adiposity and are greatly overexpressed in obesity (22). TNFα not only opposes the recruitment/differentiation of new adipocytes but also leads to dedifferentiation of mature adipocytes; furthermore, in many cell types TNFα can induce cell death. Thus some mechanism allows excess adipose tissue to persist in spite of these adipolytic signals. Obesity is usually accompanied by hyperinsulinemia and often by noninsulin dependent diabetes mellitus. Insulin is a strong adipogenic signal and is here shown to exert a protective effect on adipocytes in the obese state. Hyperinsulinemia may therefore act to preserve adipose tissue in the obese state."

"Although dramatic adipocyte cell death was only observed in obese mice, it is possible that insulin plays a subtler role in the regulation of adipocyte death even in normal individuals. Normal mice treated with streptozotocin lose the ability to secrete insulin and become diabetic (21). This is accompanied by a rapid loss of adipose tissue that has generally been attributed to lipolysis. However, in the light of this effect, the more prolonged loss of insulin in this condition may also result in adipocyte cell death. Adipocyte cell death has also been shown to occur during human weight loss. Recent reports have demonstrated that adipocyte loss can occur by apoptotic cell death and have suggested apoptosis as a mechanism in weight loss (28, 29). Among the other changes that occur during weight loss is a significant reduction in serum insulin and this may play a role in the adipocyte loss."

[LarsLasr]

I denna artikel antyder dom att det är möjligt, men säger inte hur. Jag tror man tappar fettceller om man går från exempelvis 150+kg till 90, dvs man återgår till det antalet man hade innan man blev fet. För den generelle koloiten med bf mellan 7-15% är det nog bara fyllnaden av fettceller som varierar, inte antalet som är genetiskt bestämt. Men det är vad jag tror :)

Abstract

Adipose tissue mass is reflected by the volume and the number of adipocytes and is subject to homeostatic regulation involving cell death mechanisms. In this study we have investigated the mechanisms of apoptosis in human preadipocytes and adipocytes that may play a role in the regulation of adipose tissue mass. We found that death receptors (CD95, TNF-related apoptosis-inducing ligand receptors 1 and 2, and TNF receptor 1) are expressed in human fat cells and that apoptosis can be induced by specific ligands. Sensitivity to apoptosis could be stimulated by an inhibitor of biosynthesis. In addition, inhibition of auto-/paracrine action of IGF-I dramatically sensitizes human adipocytes for death ligand-induced apoptosis. Phosphoinositide 3-kinase and, to a weaker extent, p38 MAPK are involved in IGF-I-mediated survival. IGF-I protects human fat cells from apoptosis by maintaining the expression of antiapoptotic proteins, Bcl-xL and Fas-associated death domain-like IL-1-converting enzyme inhibitory protein. In conclusion, we identified mechanisms of apoptosis induction in human fat cells. We furthermore demonstrate that human fat cells protect themselves from apoptosis by IGF-I in an auto-/paracrine manner.

IN ADDITION To its primary function of energy storage, white adipose tissue plays significant roles in metabolic regulation and overall energy homeostasis, and in part regulates satiety and insulin sensitivity (1). Adipose tissue mass is determined by competing processes regulating both the volume and the number of adipocytes. Increases in adipose tissue mass can result from an increase of the volume of adipocytes. Furthermore, adipocyte number may increase due to proliferation and differentiation of adipocyte precursor cells, which are found in large amounts in adipose tissue (2). Alternately, a reduction in fat tissue mass generally involves the loss of stored lipids by lipolytic processes. A reduction of the number of adipocytes may also be seen, especially in conditions where large amounts of fat are lost (3, 4).

Inhibition of Death-Receptor Mediated Apoptosis in Human Adipocytes by the Insulin-Like Growth Factor I (IGF-I)/IGF-I Receptor Autocrine Circuit (http://endo.endojournals.org/content/145/4/1849.full)

[massakay]

En fettcell kan svälla med upp till 1000 gånger sin egen storlek, Så det kan knappast behövas skapas fler fettceller för att få rum med mer fett än så.
Jag har för mig att dom fettcellerna man har, har man livet ut.. Varken fler eller mindre... Rätta mig gärna om jag har fel!!:)

[Eddie Vedder]

I regel ökar bara fettcellernas storlek. Men hyperplasi är inte omöjligt. Och det är knappast vad man kan kalla för nya rön. Det har ju varit känt länge.

Body fat and adipose tissue fatcell size and number were determined in a group of obese patients and in controls. These variables were analyzed at different degrees of obesity and compared with metabolic variables, including blood glucose and plasma insulin during glucose tolerance testing and blood lipids. Fatcell size was responsible for the increase of obese adipose tissue at a moderate degree of obesity. With more severe obesity, fatcell number becomes increasingly important and dominates as a factor contributing to obesity. Under conditions of unrestricted diet and activity, plasma insulin correlated positively with fatcell size but not with body fat, and tended to show a negative correlation with fatcell number. The factor in adipose tissue associated with plasma insulin increase is thus probably the fatcell size. The results suggest two forms of obesity. One is characterized by a hypertrophy of fatcells and is of a moderate degree (hypertrophic obesity). This type of obesity is associated with metabolic disturbances. Increased fatcell size might not be a primary factor in this form of obesity, but rather another symptom of metabolic disturbance. The other form (hyperplastic obesity) has an increased number of fatcells and is associated with much more severe obesity, particularly since fatcell size is often increased also in these patients.

Number and size of adipose tissue fat cells in relation to metabolism in human obesity. Metabolism. 1971 Jul;20(7):703-13.

[King Grub]

Here we show that adipocyte number is a major determinant for the fat mass in adults. However, the number of fat cells stays constant in adulthood in lean and obese individuals, even after marked weight loss, indicating that the number of adipocytes is set during childhood and adolescence. To establish the dynamics within the stable population of adipocytes in adults, we have measured adipocyte turnover by analysing the integration of 14C derived from nuclear bomb tests in genomic DNA6. Approximately 10% of fat cells are renewed annually at all adult ages and levels of body mass index. Neither adipocyte death nor generation rate is altered in early onset obesity, suggesting a tight regulation of fat cell number in this condition during adulthood.

http://www.nature.com/nature/journal/v453/n7196/full/nature06902.html

[Akada]

När menar de man slutar vara en 'adolescent', slutet av tonåren?