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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperglycemia (experimental diabetes) was induced in adult male rats by destruction of the pancreatic beta cells with a single intravenous injection of streptozotocin (STZ). Testes from diabetic, from insulin-treated diabetic, and from sham-injected normal rats were fxed by vascular perfusion. The fine structure of Leydig cells was examined at two, three, and four weeks after the STZ injection in the untreated diabetic animals, and at four weeks in the controls and insulin-treated diabetic rats. A number of morphological changes was observed in Leydig cells of untreated diabetic animals. Most obvious of these was an accumulation of lipid droplets, not normally present in Leydig cells in adults of this species. Smooth endoplasmic reticulum (SER) was markedly reduced in Leydig cells of the hyperglycemic rats. Several types of intracellular bodies were seen exclusively in Leydig cells of the untreated diabetic animals. Many resembled secondary lysosomes or dense bodies, while others appeared to be autophagic vacuoles. In addition, a small, granule-containing lamellar structure was seen either within a typical dense body or free in the cytoplasm. Myelin-like structures were commonly observed within the cytoplasm of the Leydig cell or within mitochondria. The appearance of the mitochondria in diabetic rats was otherwise normal. The extracellular spaces surrounding Leydig cells from untreated hyperglycemic rats also contained large accumulations of myelin-like material. These structural changes appear to be direct consequences of the diabetic state of the animals, since the ultrastructure of insulin-treated diabetic rats did not differ from that of the controls. These findings may reflect an alteration or breakdown of Leydig cell components normally involved in the synthesis of androgen, and correlate with previous reports of lowered circulating levels of testosterone in diabetic rats.
Anat Rec 1979 Nov
PMID:Ultrastructural changes in Leydig cells of streptozotocin-induced diabetic rats. 22 65

Both the NZW and NZB mice exhibit an elevated fasting blood sugar level when compared to Swiss white mice. The NZB/NZW F1 hybrid mouse shows still a higher fasting serum glucose level than either of its parental strains. The elevated glucose level is noted very early in the animals' life, long before definitive signs or symptoms of pathology are evident, and remains elevated at least until the fortieth week of life, the last testing period in our series before sacrificing the aminals. There are two major peaking periods for the glucose levels, namely at 4-10 weeks of age and then again at 31-40 weeks of age. These age periods correspond to the very young animal and to the animal that is beyond its prime and most likely sick and near the end of its lifespan due to the animals' inherent disease processes. The NZB and NZB/NZW F1 hybrid succumb to their disease processes at approximately 8-10 months of age. The NZW usually lives until 18 months. The questions are raised: does the altered immunologic state in the NZB and/or the NZB/NZW F1 hybrid produce the elevated blood sugar levels and the pancreatic histopathology or is it the early hyperglycemic condition coupled with pancreatic pathology which are in some measure instrumental in producing the lesions discussed and observed, in the beginning of the three to four month period of age, in the various organs? Is there a relationship between the hyperglycemic condition and the immune state or are these independent phenomena in a genetically "mixed up" mouse?
Anat Rec 1975 Aug
PMID:Hyperglycemia in the NZB/NZW F1 hybrid mouse. 114 91

The conducting airway epithelium of fetal Syrian golden hamsters was studied from gestational day 12 to day 15, during normal and uncontrolled diabetic pregnancies. Diabetes was induced in the pregnant hamsters by injecting streptozotocin at 60 mg/kg body weight, subcutaneously, early on gestational day 10. Cells in S-phase were labelled immunochemically with bromodeoxyuridine (BrdU), and the day on which endocrine cells and ciliated cells first appeared was determined. In control fetuses, the BrdU-labelling indices (LI's) of different anatomical airway levels were significantly different from one gestational day to the next. For example, the LI of the lobar bronchus was significantly different on each gestational day (P less than .0001), and the same was true of the bronchioles. Moreover, the difference between LI's of the lobar bronchus and bronchioles-terminal buds was highly significant on day 12 (P less than .0001), and on day 13 the differences between lobar bronchus and bronchioles, lobar bronchus and terminal buds, and bronchioles and terminal buds were also highly significant (P less than .0001). However, on gestational days 14 and 15, the LI's were reduced and were comparable at different airway levels. The BrdU-labelling indices were very consistent among fetuses of the same age, and the differences between the average LI's for pups of different litters was numerically very small. Hyperglycemia (mild, moderate, severe) did not alter LI's in the fetal airway epithelial cells. Furthermore, although glycogen was not depleted from the airway epithelium of the hyperglycemic fetuses as it was in the controls, the endocrine cells first appeared on gestational days 12, 13, and 14, respectively, in the trachea, lobar bronchus and bronchioles, followed 1 day later by the ciliated cells, in the fetuses of control and diabetic mothers. In our experimental model, induction of diabetes in the pregnant hamsters on gestational day 10 did not appear to alter development or differentiation of the fetal conducting airway epithelium.
Anat Rec 1990 May
PMID:Development of the conducting airway epithelium in fetal Syrian golden hamsters during normal and diabetic pregnancies. 236 22

The modulating effects of estradiol (E: 1 microgram/3.5 days) and progesterone (P: 2 mg/3.5 days) on the obesity and hyperinsulinemic and hyperglycemic components of the diabetes-obesity syndrome in female C57BL/KsJ (db/db) mice, which includes cellular atrophy and adiposity in the reproductive tract, were examined and compared to corresponding control (+/?) parameters. All control and diabetic mice received oil (vehicle control), E, or P treatments starting at 4 weeks of age. Body weight, serum insulin levels, blood glucose concentrations, and utero-ovarian lipoprotein lipase activities were analyzed at 8 and 16 weeks of age and related to the ultrastructural changes in the steroid-sensitive uterine epithelium during the treatment period. Neither E nor P had any effect on body weights in (+/?) or (db/db) mice. The pronounced diabetes-associated elevation in serum insulin levels was enhanced by E, and suppressed by P, in 16-week-old (db/db) mice as compared with controls. By 16 weeks of age, the E therapy normalized blood glucose levels in diabetic mice to control levels, whereas P was ineffective in modulating the hyperglycemia. The reduction in blood glucose levels in E-treated diabetic mice correlated temporally with the return of normal intracellular structure including the disappearance of intracellular lipid vacuoles characteristic of uterine epithelium cells of (db/db) mice. The diabetes-induced rise in utero-ovarian lipoprotein lipase activity was normalized by P-therapy. The reduction in utero-ovarian lipoprotein lipase activity coincided temporally with the demonstrated intracellular reorganization in (db/db) reproductive tract tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
Anat Rec 1989 Dec
PMID:Effects of estradiol and progesterone on diabetes-associated utero-ovarian atrophy in C57BL/KsJ (db/db) mutant mice. 268 92

The effects of the diabetes (D) mutation on utero-ovarian structure and function were examined in match-paired D and control (C) C57BL/KsJ mice between 2 and 16 weeks of age. Between 4 and 8 weeks of age, the uterine epithelium of D mice exhibited a remarkable increase in the amount of cytoplasmic lipid stores as compared with that of C animals. Associated with progressive hyperglycemia between 8 and 16 weeks of age, uterine atrophy and continued lipid accumulation occurred. Both serum progesterone and estradiol levels were lower in D than C mice between 8 and 16 weeks of age. In addition, the uteri of D mice failed to accumulate as much 3H-estradiol as C uteri at 16 weeks of age. These data demonstrate that changes in uterine structure that are attributable to depressed ovarian activity in diabetics underlie the reproductive failure in these animals. The temporal association between the onset of reproductive tract involution and the expressed hyperglycemic condition suggests a causal association between these events in the genetically diabetic C57BL/KsJ mouse.
Anat Rec 1985 Apr
PMID:Diabetes-associated alterations in uterine structure in the C57BL/KsJ mouse: relationship to changes in estradiol accumulation, circulating ovarian steroid levels, and age. 399 90

The effect of the progressive hyperglycemic condition on ovarian follicular maturation was studied in control, moderate (160-350 mg/dl blood glucose), and overt (greater than or equal to 350 mg/dl blood glucose), spontaneously diabetic Chinese hamsters. Match-paired (age, sex, and weight) control and diabetic animals were sacrificed at specific intervals during the development of the diabetic condition; the ovaries were collected and morphometrically analyzed for changes in ovarian follicular growth relative to blood glucose levels. Follicles were classified according to size, number, and condition. The total number of primary (100-200 micrometers diameter) and secondary (200-350 micrometers diameter) follicles was reduced in both moderate and overt diabetic females as compared with controls. The percentage of viable (i.e., nonatretic) follicles was greatly reduced in the secondary follicle class of overt diabetic animals as compared with controls. No significant differences were observed in the numbers of viable tertiary (i.e., greater than or equal to 350 micrometers diameter) follicles in any of the diabetic animals as compared with controls. The percentage of atretic, secondary follicles was greatly increased in the overt diabetic group as compared with controls. These data indicate that the progressive hyperglycemia associated with diabetes in the Chinese hamster induces a severe depression of normal follicular recruitment resulting in an impaired reproductive performance in this species.
Anat Rec 1984 Nov
PMID:Effects of progressive hyperglycemia on ovarian structure and function in the spontaneously diabetic Chinese hamster. 652 90

Although there is a recent increase in the use of the isolated pancreatic islets of the rat in the transplantation and functional studies, there has been no detailed quantitative assessment on the size and cellular constituents of islets after the isolation procedure. The present work was undertaken to study the size classes of the isolated islets and the morphometry of their cellular populations. Islets of the rat pancreas were isolated by using the intraductal collagenase digestion technique, the most commonly used procedure for the isolation of pancreatic islets. Different endocrine cells of the isolated islets were stained by immunoperoxidase staining techniques. The distribution of the cellular constituents of the isolated islets was similar to that of the intact islets of the normal pancreas; A, D, and PP cells were peripherally arranged around the centrally located B cells. However, morphometric quantitative study showed that the percent volume and percent number of A, D, and PP cells of the isolated islets were lower than those of the corresponding intact ones. Further, the mean true diameter of the isolated islets was lower than that of the intact ones. These data indicate loss of islet cells during the process of isolation. Most of the lost cells were from the periphery of islets. This may provide an explanation for the incomplete metabolic control and recurrence of hyperglycemia encountered after isolated islet transplantation in the treatment of diabetes mellitus. It seems that further refinements of the isolation techniques are necessary to obtain islet tissue with total cellular integrity, before a complete success in transplantation could be achieved.
Anat Rec 1993 Dec
PMID:Isolated pancreatic islets of the rat: an immunohistochemical and morphometric study. 790 7

We investigated the possible relationship between islet amyloid polypeptide (IAPP) and the hyperinsulinemia and/or hyperglycemia that is seen in the desert-adapted gerbil Psammomys obesus, when the animal is transferred from a low-energy (LE) diet to a high-energy (HE) diet. The effects of vanadyl sulfate and transition from a HE to a LE diet on the diabetic state of the Psammomys were also studied. Psammomys maintained on a LE diet, showing normoinsulinemia and normoglycemia (group A), were used as controls. IAPP and insulin immunoreactivity in the islets of Langerhans was studied using the peroxidase-antiperoxidase technique and plasma levels of the two hormones were determined by radioimmunoassays. The islet immunoreactivity of both IAPP and insulin was significantly weaker in the hyperinsulinemic and hyperglycemic Psammomys (group C) compared to group A. Transfer to a LE diet resulted in complete recovery of the IAPP- and insulin-staining pattern to that seen in group A [group A--Rec (nutrition)]. The plasma IAPP levels of the group C animals were not significantly higher than in group A, while after vanadyl sulfate treatment the IAPP levels and IAPP/insulin ratios remained significantly higher [group A--Rec (vanadyl)]. At the same time the circulating levels of glucose and insulin were restored to normal. Conclusively, islet IAPP and insulin immunoreactivity disappeared and reappeared in parallel in Psammomys transferred to a HE diet and back to a LE diet. Furthermore, vanadyl sulfate treatment of the hyperinsulinemic and hyperglycemic animals normalized circulating glucose and insulin levels, but not IAPP levels, possibly due to a negative feedback effect of IAPP on insulin release.
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PMID:Islet amyloid polypeptide in Psammomys obesus (sand rat): effects of nutritionally induced diabetes and recovery on low-energy diet or vanadyl sulfate treatment. 936 Oct 89

Capillary basement membrane (CBM) thickening is an ultrastructural hallmark in diabetic patients and in animal models of diabetes. However, the wide variety of tissues sampled and diverse methods employed have made the interpretation of thickness data difficult. We showed previously that acellular glomerular BMs in OVE26 transgenic diabetic mice were thickened beyond normal age-related thickening, and in the current study we hypothesized that other microvascular BMs likewise would show increased widths relative to age-matched controls. Accordingly, a series of tissues, including skeletal and cardiac muscle, ocular retina and choriod, peripheral nerve, lung, pancreas, and renal glomerulus was collected from 300-350-day-old normal and transgenic mice. Transmission electron micrographs of cross sections through capillary walls were prepared, and CBM thickness (CBMT) was determined by the "orthogonal intercept" method. Morphometric analyses showed highly variable transgene-related BMT increases in the sampled tissues, with glomerular BM showing by far the greatest increase (+87%). Significant thickness increases were also seen in the retina, pulmonary alveolus, and thoracoabdominal diaphragm. BMT increases were not universal; however, most were modestly widened, and those that were thickest in controls generally showed the greatest increase. Although the pathogenesis of diabetes-related increases in CBM is poorly understood, data in the current study showed that in OVE26 transgenic mice increased BMT was a frequent concomitant of hyperglycemia. Accordingly, it seems likely that hyperglycemia-induced microvascular damage may be a contributing factor in diabetic BM disease, and that microvessel cellular and extracellular heterogeneity may limit the extent of CBM thickening in diverse tissues.
Anat Rec A Discov Mol Cell Evol Biol 2003 Apr
PMID:Ultrastructural morphometry of capillary basement membrane thickness in normal and transgenic diabetic mice. 1262 76

Following liver transplantation, all hepatic nerves are transected; thus, liver allografts are completely isolated from neural control of their hosts. Despite this absolute denervation, liver allograft function does not appear to be significantly impaired after successful transplantation. In experimental animal models, hepatic denervation has no major effects on bile acid production and biotransformation, while it increases blood pressure and salt retention; decreases the number of hepatic progenitor cells, cholangiocyte proliferation, and liver regeneration; and influences the hepatic microcirculation, diet behavior, and glycemic control. In humans, hepatic denervation after liver transplantation has no major deleterious effects on bile secretion, liver regeneration, and hepatic blood flow. Insulin resistance and postprandial hyperglycemia, changes in ingestion behavior, and reduced stimulation of hepatic progenitor cells in the canals of Hering are the major side effects of absent liver innervation. Despite these abnormalities, patients can lead a new life with improved quality of life.
Anat Rec A Discov Mol Cell Evol Biol 2004 Sep
PMID:Transplanted liver: consequences of denervation for liver functions. 1538 9


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