Wat denken jullie hierover?

[Falstyr]

Interessant stukje. Maar ik meen dat vetcellen zich wel degelijk konden delen. Volgens dit verhaal kan dat dus niet. Leuk.

Heb nooit iets vernomen over vetcellen die konden delen. Wel dat ieder persoon afhankelijk van zijn lichaamstype een x-hoeveelheid vetcellen had. Een endo heeft er aanzienlijk meer. Als de vetcellen vol zijn zal het lichaam zelf nieuwe aanmaken als meer opslag, want elke vetcel heeft een bepaalde hoeveelheid die het kan opnemen. Nadeel is dat de nieuwe aangemaakte hoeveelheid cellen nooit minder zullen worden ongeacht wat je zal doen.

[GeneralIx]

Lees dit eens:

02-25-2004, 02:18 PM
I haven't come across any of the more promising studies regarding decreases in adipocyte numbers (either effectively artificially induced or naturally), so I'll be on the lookout for those.

Most bodily cells grow old and die, but they eventually regenerate, so do fat cells not follow these sequence of events? This has been, more or less, the topic of the past and recent articles I've been reading, one of which studied the aging process of mature adipocytes in simulated tissue environments. These adipocytes displayed catabolic functioning as evidenced by aging biomarkers, including slowed metabolisms, but the most important thing never faltered -- aged adipocytes remained steadfast in their ability to store and hold on to fats.

Not to worry, though, other studies have shown that the hormone leptin can kill off adipocytes, aged or not. This effect has been shown in rats who had leptin chronically injected into an area of the brain (so even though leptin is naturally produced by adipocytes, its ability to cause cell death without the aid of whatever the CNS is doing, is limited. Or, its ability is dependent on the size or age of the adipocyte, or some other factor). Besides the rats who died shortly after the injections, all the rest of them showed definite cell size decreases, but the leptin consistently discriminated against the elimination of certain types of adipose cells.

Furthermore, in a review article a few years ago on how the body (animals and humans) regulates its total fat stores, when fat cells were taken out of rats, the original numbers were always regained. What was also interesting was that this restoration of cell number was not always dependent on an increase in food intake. These results, which have been duplicated using different species, seem to indicate that whatever the fat-regulating mechanisms are, it's strongly biased toward having a certain amount of body fat.

Of course, the results regarding fat cell numbers obtained from animal studies and from adipose tissue cultures can't be accurately extrapolated to humans. However, there has been research on humans pointing to only reductions in adipocyte volumes while the total number of adipocytes remain near constant, regardless of the fat loss method. I can't elaborate any more, as the details of these studies elude me at the moment. But if there are displays of absolute interest, I'll look them up.

Yes, it would be nice if fat cells died and never came back, and science may one day gain a greater understanding of the interactions between adipocytes and its regulation within the larger system, but I wouldn't put too much into waiting for a "cure" for weight problems.

Well, I just wanted to address some of the ideas raised in the post above mine, because I find this to be an interesting topic with many implications. And obviously, I've addressed only a very tiny part of all the data that exists in this area.

Bron.

En het vetcellen delen verhaal had ik van T-Nation, maar zal verder zoeken.

En er is meer: hyperplasia van de vetcellen bij muizen:

Adipose cell hyperplasia and enhanced glucose disposal in transgenic mice overexpressing GLUT4 selectively in adipose tissue.Shepherd PR, Gnudi L, Tozzo E, Yang H, Leach F, Kahn BB.
Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts.
To gain insight into the molecular pathogenesis of obesity and specifically the role of nutrient partitioning in the development of obesity, we overexpressed the insulin-responsive glucose transporter (GLUT4) in transgenic mice under the control of the fat-specific aP2 fatty acid-binding protein promoter/enhancer. Two lines of transgenic mice were generated, which overexpressed GLUT4 6-9-fold in white fat and 3-5-fold in brown fat with no overexpression in other tissues. In vivo glucose tolerance was enhanced in transgenic mice. In isolated epididymal, parametrial, and subcutaneous adipose cells from transgenic mice, basal glucose transport was 20-34-fold greater than in nontransgenic littermates. Insulin-stimulated glucose transport was 2-4-fold greater in cells from transgenic mice. Total body lipid was increased 2-3-fold in transgenic mice overexpressing GLUT4 in fat. Surprisingly, fat cell size was unaltered and fat cell number was increased > 2-fold. This is the first animal model in which increased fat mass results solely from adipocyte hyperplasia and it will be a valuable model for understanding the mechanisms responsible for fat cell replication and/or differentiation in vivo.
PMID: 8226728 [PubMed - indexed for MEDLINE]

Bron.