Sunday, 29 May 2016

adipose controls appetite

Compensatory growth of adipose tissue after partial lipectomy: involvement of serum factors.

The regulation of body weight/fat was studied by investigating mechanisms for compensatory adipose tissue growth after removal of bilateral epididymal fat pads from male adult Wistar rats. Food intake during the first 4 weeks and energy expenditure on Days 8-10 postsurgery were not different between lipectomized and sham operated rats. During Days 29-31 post surgery, a small (2.4%) but significant (P < 0.05) increase in heat production per metabolic body size was detected in lipectomized as compared with sham operated rats. The carcass composition of lipectomized and sham operated rats was not significantly different 16 weeks after surgery. The compensatory growth was fat pad-specific: mesenteric, retroperitoneal, and inguinal fat pads, but not perirenal fat pads, were heavier in lipectomized rats than in sham operated rats as early as 4 weeks postsurgery. Examination of fat cell size distribution in the compensating pads indicated a shift toward larger cells in retroperitoneal fat, but not in inguinal fat of lipectomized as compared with sham operated rats. Serum from lipectomized rats, but not media conditioned by exposure to retroperitoneal fat pads from lipectomized rats, stimulated proliferation of preadipocytes in vitro more than that from sham operated rats. Thus, compensatory adipose tissue growth after lipectomy may be mediated, in part, by blood-borne factors that are derived from tissues other than adipose tissue.

Food intake and energy expenditure measurements
focused on the early period up to 4 weeks postsurgery
and did not detect measurable increases in food intake or
decreases in energy expenditure that could account for the
lipid deposition associated with compensatory growth.

lol CICO?

Relationship of adipocyte size to hyperphagia in developing male obese Zucker rats.

In growing male obese Zucker rats, hyperphagia reaches a maximum or "breakpoint" and declines at an earlier age with high fat than with chow-type diets. A serial adipose tissue biopsy technique was used to correlate changes of retroperitoneal adipocyte size and feeding behavior in 5- to 7-wk-old male lean and obese rats fed laboratory chow or a 35% fat diet until 30 wk of age. Although chow-fed groups had significantly greater cumulative intake, fat-fed groups had significantly greater body weight gain, retroperitoneal depot weight, and adipocyte number. Mean adipocyte size increased continuously in chow-fed groups but decreased over weeks 20-30 in fat-fed groups, reflecting increased adipocyte number. In fat-fed obese rats, hyperphagia reached a breakpoint at 11 wk and disappeared by 13 wk. In chow-fed obese rats, hyperphagia reached a breakpoint at 15-16 wk and disappeared by 19 wk. Biopsy samples revealed that adipocyte size of fat-fed obese rats was already close to maximal at 10 wk (1.12 micrograms lipid), while that of chow-fed obese rats only approached maximal at 20 wk (0.81 microgram lipid). At these time points, lipoprotein lipase activity paralleled adipocyte size. These data indicate that the duration of the growing obese rat's hyperphagia coincides with adipocyte filling and suggest the existence of feeding stimulatory and inhibitory signals from adipose tissue.

So again more evidence adipose tissue is controlling appetite and since this is in zucker rats something other than leptin is involved.


  1. Hi Kindke,
    from the second study:

    It is of interest to note that both lean and obese high fat-fed groups in the present study, while consuming total fewer calories, had significantly greater body weight gains and adipocyte numbers than chow-fed groups.

    Fewer calories, greater weight gain. Cause? The diet is obesogenic.



    1. indeed

      im really on a mission at the moment to try and show/prove my theory that it is adipose tissue driving appetite especially in obese, I.E. somehow when the adipose tissue needs to fill or get bigger or when it is growing it increases host appetite through yet undetermined mechanisms.

      consequently I might speculate that the spontaneous reduction in appetite on low-carb is due to the adipocytes attempting to empty themselves ( weight loss )

    2. basically somehow adipose tissue is controlling appetite outside of just leptin im really sure of it.