[Effects of aging associated with weight gain on the cell size and heterogeneity of different fat depots in the rat]

The mass of adipose tissue expands during weight gain mostly because of an increase in fat cell diameter, which is one of the most important determinants of tissue metabolism. The aim of this study was to examine the effects of aging associated with weight gain on cell size and heterogeneity of adipocytes at different fat depots. Adipose tissues were harvested from subcutaneous [SC], retroperitoneal [RP], perirenal [PR], proximal epididymal [PE] and distal epididymal [DE] regions of two groups of rats with a 30-day difference in age and 36% increase in body weight. Diameters of fat cells were measured using a microscope equipped with a calibrated micrometer. Cell size heterogeneity was deduced from coefficients of variation. In both groups, no significant regional differences were observed in diameter of adipocytes in various fat depots. With the exception of the RP depot, the weight gain caused a significant increase in diameter of adipocytes in all other depots. The highest and the lowest increase were seen in PR and RP adipocyte diameter, respectively. The degree of heterogeneity of fat depots was not significantly altered by weight gain. Aging associated with weight gain leads to fat cell hypertrophy in a depot specific manner, and cells at depots close to survival organs such as kidney and gonads are more affected than those of the other depots. The results of this study can enhance current knowledge on adipose tissue mass expansion and its related health complications such as cardiovascular diseases and diabetes

TGF-beta1 latency associated peptide promotes remodeling of healing cutaneous wounds in the rat

The process of wound healing involves integrated events including inflammation, granulation tissue formation, matrix deposition and remodeling. Growth factors play a key role in the process. Among them transforming growth factor-beta1 [TGF-beta1] is known to accelerate tissue repair by promoting the synthesis and deposition of extracellular matrix proteins. However, persistence or overactivity of TGF-beta1 during the remodeling phase can potentially lead to fibrosis. The primary objective of this study was, therefore, to determine the effects of TGF-beta1 inactivation, by its latency associated peptide [LAP], on the cutaneous healing wounds. Excisional wounds were generated on the back of male adult rats. Wounds received TGF-beta1 or LAP during the post-inflammatory phase. Expression of type I collagen and - smooth muscle actin was evaluated by Western blotting. Wound maturation was further assessed by histology and immunohistochemical methods using specific antibody for proliferating cell nuclear antigen [PCNA]. Wounds treated with TGF-beta1 showed a marked increase in the level of type I collagen, whereas no significant changes were observed in the wounds treated with LAP as compared to that in control. Expression of -smooth muscle actin was markedly reduced in the wounds treated with LAP but was slightly increased in the wounds treated with TGF-beta1. Both neodermis and newly-formed epidermis exhibited a higher degree of maturation in the LAP-treated wounds as compared to TGF-beta1 treated wounds. Local administration of LAP seems to be beneficial to tissue remodeling. It promotes wound maturation and, may prevent fibrosis and hypertrophic scarring

effect of opium on glucoregulatory factors

Effects of opium, morphine and demorphinized opium were studied on the blood sugar, liver glycogen and serum insulin level in rats. Demorphinized opium as well as morphine increased blood sugar levels and the results were similar to those of rats receiving opium. Rats receiving opium or morphinehydrochloride showed a severe terminal hypoglycemia, which was not seen in those receiving demorphinized opium. The liver glycogen contents and serum insulin levels were higher in opium or demorphinized opium treated rats compared to the controls. The above results suggest that the other opium alkaloids might differ from morphine in their effects on the glucoregulatory factors