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Query: UMLS:C0011849 (diabetes)
 277,896 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

Osteopenia is a recognized complication of diabetes mellitus in humans and experimental animals. We recently found that tetracyclines prevent osteopenia in the streptozotocin-induced diabetic rat and that this effect was associated with a restoration of defective osteoblast morphology (Golub et al., 1990). The present study extends these initial ultrastructural observations by assessing osteoblast function in the untreated and tetracycline-treated diabetic rats. After a 3-week protocol, non-diabetic control and diabetic rats, including those orally administered a tetracycline, minocycline (MC), or a non-antimicrobial tetracycline analog (CMT), were perfusion-fixed with an aldehyde mixture; the humeri were dissected and processed for ultracytochemical localization of alkaline phosphatase (ALPase) and Ca-ATPase activities. Some rats from each experimental group received an intravenous injection of 3H-proline as a radioprecursor of procollagen, and the humeri were processed for light microscopic autoradiography. In addition, the osteoid volume in each experimental group was quantitatively examined by morphometric analysis of electron micrographs. During the diabetic state, active cuboidal osteoblasts in the endosteum of control rats were replaced by flattened bone-lining cells that contained few cytoplasmic organelles for protein synthesis (Golgi-RER system), and active transport (mitochondria). Treating diabetic rats with MC, and even more so with CMT, appeared to "restore" osteoblast structure. During diabetes, bone-lining cells incorporated little 3H-proline or secreted little labeled protein and produced only a very thin osteoid layer. Tetracycline administration to the diabetics increased both the incorporation of 3H-proline by osteoblasts and their secretion of labeled protein toward the osteoid matrix, in a pattern similar to that seen in the non-diabetic controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Anat Rec 1991 Sep
PMID:Tetracycline administration restores osteoblast structure and function during experimental diabetes. 183 18

The present study analyzes the regeneration of skeletal muscle in diabetic rats. Intravenous injection of streptozotocin (STZ) was used to induce diabetes. Six weeks later the extensor digitorum longus (EDL) muscles from diabetic rats were either transplanted into diabetic or normal hosts to initiate regeneration. Normal EDL muscle transplants in normal and diabetic hosts were also performed for comparison. One, 2, 4, and 12 weeks after transplantation, the EDL regenerates were morphologically analyzed. Regeneration and formation of neuromuscular junctions were observed in all transplants, including diabetic regenerates in diabetic hosts. The overall mass and myofiber size of the diabetic EDL regenerate in the diabetic host was significantly reduced in spite of complete regeneration. Recovery of the diabetic muscle mass and the myofiber size was observed after transplantation into normal hosts. A reduction in mass and myofiber size was observed in normal EDL muscles transplanted into diabetic hosts. It is concluded that poor recovery of diabetic muscle is related to metabolic and structural alterations in the diabetic host, rather than to innate capacity of the muscle to per se undergo regeneration and reinnervation. The observed enhancement in recovery of diabetic muscle after transplantation in a normal host and deterioration of normal muscle after transplantation in a diabetic host shows that the host environment determines the success of muscle regeneration.
Anat Rec 1991 Mar
PMID:Regeneration of skeletal muscle in streptozotocin-induced diabetic rats. 202 74

Diabetes induces osteopenia, which is characterized by a deficiency of osteoid and decreased activity of osteoblasts. We recently found that tetracyclines prevent the loss of osteoid and bone matrix and the degeneration of osteoblasts in diabetic rats by a mechanism independent of their antimicrobial efficacy. However, bone remodeling requires the activity of osteoclasts as well as osteoblasts. To determine the in vivo effects of tetracycline on osteoclasts in long bones, either a tetracycline (minocycline, TC) or its chemically modified non-antibiotic analogue (CMT), 4-de-dimethylaminotetracycline, was administrated daily to streptozotocin-induced diabetic rats by oral intubation. After 21 days, the rats were perfusion-fixed with a mixture of formaldehyde and glutaraldehyde, and the humeri were dissected and processed for ultracytochemical demonstration of acid trimetaphosphatase (ACPase) activity. In untreated non-diabetic (control) rats, the osteoclasts at the zone of provisional ossification exhibited abundant mitochondria and cisterns of rough endoplasmic reticulum (RER) throughout the cytoplasm, prominent stacks of Golgi membranes, and lysosomes in the perinuclear cytoplasm, and numerous various pale vacuoles in the cytoplasmic area adjacent to well-developed ruffled border. Intense ACPase activity was observed in the Golgi saccules, lysosomes, pale vacuoles, and the extracellular canals of ruffled border. The reaction products were also noted along the resorbing bone surfaces associated with the osteoclast ruffled border. The osteoclasts in the untreated diabetic rats showed a cytoplasmic organization similar to that of the non-diabetic control rats, but showed little or no ruffled border which was replaced by a broad clear zone in some of these cells. However, most of the osteoclasts on bone matrix in the diabetics were devoid of both a ruffled border and a clear zone. ACPase activity was detected in the osteoclast cytoplasm of diabetic rat, as in the controls, but to a much lesser extent along the broad clear zone facing the resorbing bone surfaces. The osteoclasts in TC-treated diabetic rats possessed both a clear zone and a small ruffled border. However, in some cases, they lacked both structures reminiscent of the untreated diabetic cells. The osteoclasts of CMT-treated diabetic rats exhibited structural and enzymatic features essentially identical to those of the non-diabetic control rats. These results suggest that the diabetes-induced osteopenia results, at least in part, from degeneration of osteoclasts (as well as atrophic osteoblasts) and that tetracyclines may be effective in preventing these abnormalities by a mechanism not dependent on the drugs' antimicrobial properties.
Anat Rec 1990 Aug
PMID:Tetracycline administration normalizes the structure and acid phosphatase activity of osteoclasts in streptozotocin-induced diabetic rats. 216 33

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

Despite the extensive literature concerning the neuropathy associated with diabetes, only limited information describes changes in the associated muscle. The objective of this study was to evaluate the histochemical and morphometric characteristics of diabetic muscle in the C57BL/KsJ db-m strain of mouse. The histochemical analysis of myofiber type for the diabetic mouse revealed that the extensor digitorum longus muscle consisted of 53.1% type 2a, 46.0% type 2b, and 0.9% type 1 myofibers, a significant shift from the percentages found in the nondiabetic litter mates (44.4% type 2a, 55.6% type 2b, no type 1). Computer-assisted morphometric analysis of myofiber size by fiber type indicated a significant difference in myofiber size for the type 2b fibers in muscles from diabetic mice. Similarly, there was a shift in the fiber size distribution to include a greater number of small type 2b myofibers when compared to controls. Skeletal muscle from diabetic mice exhibited a significant change in the percentage of fiber types, with an increase in the number of type 2a fibers, a fiber type grouping that implies possible denervation and reinnervation, and a decrease in myofiber size. These findings may explain why some diabetic patients complain of muscle weakness.
Anat Rec 1989 Sep
PMID:Skeletal muscle in the diabetic mouse: histochemical and morphometric analysis. 277 12

The use of the streptozotocin rat model for diabetes has been questioned by the appearance of extrapancreatic cytotoxicity, notably renal and hepatic. In this study the model was made specific to diabetic, drug-induced, and starvation effects on parameters of testicular histology. Formulation of orthogonal contrast expressions permitted the statistical separation of these influences. Tubules from moderately diabetic animals showed frequent thinning, and premature desquamation of pachytene spermatocytes and early spermatids from the germinal epithelium. Results showed that only diabetes significantly decreased seminiferous tubule diameter and increased testicular blood vessel numbers. In addition, significant alteration from the control pattern of tubule stage distribution was noted, particularly at stages IX-XI. Due to the inclusion of a drug-treated but nondiabetic group, streptozotocin itself was shown to have no significant effect on these parameters.
Anat Rec 1986 Apr
PMID:Testicular histology in streptozotocin-induced diabetes. 293 78

Salivary gland striated duct cells play an important role in the modification of primary saliva by secretion and reabsorption of electrolytes, and secretion of glycoproteins. Recent observations have shown that in the rat parotid gland these cells are able to internalize exogenous proteins, e.g., horseradish peroxidase and ferritin, from the ductal lumen. In rats made diabetic by injection of streptozotocin, dense vacuoles and crystalloids are present in the apical cytoplasm of parotid striated duct cells. In this study we utilized electron microscopic immunocytochemistry to determine if these vacuoles and crystalloids contain acinar secretory proteins. At various times after induction of diabetes by streptozotocin (65 mg/kg), the parotid glands were fixed in a glutaraldehyde-formaldehyde mixture, postfixed in OsO4, and embedded in epoxy resin. Thin sections were immunolabeled with antibodies to protein B1 (Ball et al., 1988) and alpha-amylase (Baum et al., 1982) using a modification of the Protein A-gold technique (Bendayan and Duhr, 1986). With antibody to B1, label was localized in the secretory granules of acinar and intercalated duct cells of both normal and diabetic rats. In striated duct cells of diabetic rats, label was present over the electron-dense vacuoles but not over the crystalloids. Since crystalloids appear to form within the vacuoles, their lack of reactivity may indicate degradation of the internalized protein. The same distribution of label was found with antibody to amylase except for the intercalated duct granules, which were unlabeled in both control and diabetic animals. These results demonstrate that striated duct cells take up salivary proteins from the lumen and that the endocytosis of some secretory proteins from the saliva may be a significant function of these cells in certain pathological conditions.
Anat Rec 1988 Aug
PMID:Endocytosis of parotid salivary proteins by striated duct cells in streptozotocin-diabetic rats. 297 65

Previous transmission electron microscopic studies have demonstrated glomerular basement membrane (GBM) thickening and mesangial matrix (MM) expansion in chronic stages of diabetes. It is difficult, however, to achieve an appreciation of GBM surface features and distribution of MM in planar views. In the current study, autopsy human renal cortical tissue from patients with end-stage diabetic nephropathy were minced and rendered acellular with detergents prior to fixation, cryofracture, and preparation for light microscopic (LM), transmission electron microscopic (TEM), and scanning electron microscopic (SEM) observation in an effort to visualize extracellular materials in three dimensions. Our studies demonstrated that although diabetic glomerular changes vary widely within and between individuals, most showed alterations primarily affecting peripheral (epithelial) GBM (with MM increased but diffusely distributed), or they exhibited similar GBM changes but with variable nodular MM expansion leading ultimately to capillary occlusion. Both types showed peripheral GBM thickening and demonstrated external surface irregularities that by SEM appeared as "cauliflower-like" lobulations. In these glomeruli, GBM lamellation or reduplication was common with internal layers frequently thrown into lumenward projections. Glomeruli with diffusely distributed MM generally showed patent capillary channels with little evidence of occlusion. By TEM, highly compact, epithelial GBMs were clearly distinguishable from the electron-lucent MM. In these preparations the matrix was concentrated in relatively small discrete masses sometimes covered by a finely fibrillar material, which extended intermittently onto lumenal surfaces of epithelial GBMs. In more advanced stages of MM involvement, glomeruli typically exhibited smooth-surfaced nodules that were increased at the expense of capillary surface area. By TEM, MM nodules were comprised of a meshwork of very fine (20-A) fibrils surrounding a variety of detergent-resistant structures including collagenous fibrils and non-collagenous 30-nm circular fibrils with 16-nm subunits. By SEM, GBM and MM nodules were not distinguishable and merged to form substantial barriers to capillary blood flow. In those capillary channels remaining patent, inwardly projecting folds and ridges were common GBM features, and frequently thin fenestrated layers, distinctly separate from epithelial GBMs, formed sieve-like linings for the channels. These three-dimensional observations provide unique views of the processes leading to diabetic glomerular occlusion and suggest a potential for this technique in the study of renal BM disease.
Anat Rec 1986 Nov
PMID:SEM studies of acellular glomerular basement membrane in human diabetic glomerulopathy. 378 17


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