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  • 1
    Electronic Resource
    Electronic Resource
    Ciglitazone, a new hypoglycaemic agent. 4. Effect on pancreatic islets of C57BL/6J-ob/ob and C57BL/KsJ-db/db mice (1984)
    Springer
    Diabetologia 27 (1984), S. 225-234 
    Details
    ISSN: 1432-0428
    Keywords: Ciglitazone ; C57BL/6J-ob/ob mice ; C57BL/KsJ-db/db mice ; β-cell granulation ; electron microscopy ; rough endoplasmic reticulum ; Golgi apparatus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Pancreases of treated and control male C57BL/6J-ob/ob and C57BL/KsJ-db/db mice were evaluated by qualitative and morphometric microscopic techniques to determine the effects of chronic ciglitazone treatment on the morphology of β cells and surface area and number of pancreatic islets. The β cells of treated ob/ob and db/db mice displayed moderate to heavy granulation whereas most β cells of untreated obese and diabetic mice were extensively degranulated. Although moderate proliferation of the rough endoplasmic reticulum and Golgi apparatus was evident in some β cells of treated db/db mice, both groups of treated ob/ob and db/db mice displayed an improved pattern of insulin synthesis and storage. In contrast, the β cells of untreated ob/ob and db/db mice were in a severe state of stress which was indicated by extensive hypertrophy of the rough endoplasmic reticulum, Golgi apparatus and mitochondria. Some β cells of untreated db/ db mice also displayed lysosome aggregates indicative of early stages of necrosis. Morphometric analysis revealed that the surface area of islets of treated ob/ob mice was significantly smaller in comparison with that of untreated ob/ob mice. Since the surface area of islets of treated C57BL/6J-+/? mice (lean littermates of ob/ob mice) was less than that of treated ob/ob mice, the progression of islet hypertrophy in the obese mice was probably arrested or attenuated but not to the level of the treated +/? mice. The number of pancreatic islets was significantly greater in treated than in untreated db/ db mice. A majority of the islets of untreated db/db mice were atrophie and consisted of acinar and endocrine cells whereas most of the islets of treated db/db mice appeared to be intact and unremarkable. The results of this study suggest that ciglitazone is an effective hypoglycaemic agent which may directly or indirectly promote β-cell regranulation and an improved pattern of insulin synthesis and storage in ob/ob and db/db mice. However, in treated db/db mice, there still was some evidence of stress in the β cells. Overall, the prolonged treatment with ciglitazone also seemed to inhibit the hypertrophy of islets in ob/ob mice and protect the structural integrity and viability of islets in db/db mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00273811
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Ciglitazone, a new hypoglycaemic agent. 3. effect on glucose disposal and gluconeogenesis in vivo in C57BL/6J-Ob/Ob and — +/? Mice (1983)
    Springer
    Diabetologia 25 (1983), S. 514-520 
    Details
    ISSN: 1432-0428
    Keywords: Ciglitazone ; C57BL/6J-ob/ob mice and their lean littermates ; glucose turnover rate in vivo ; gluconeogenesis in vivo ; Cori cycle
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ciglitazone is orally active in preventing and reversing the hyperglycaemic syndrome in C57BL/6J-ob/ob mice and it is only mildly and transiently hypoglycaemic in lean littermates (C57BL/6J- +/?). Its effect on glucose disposal in vivo was estimated by injecting glucose-6-3H/14C and following the specific activity of radiolabelled glucose at 15, 30, 45, and 60 min after injection. The rate constants of glucose turnover were calculated to be as follows in decreasing order: treated obese (0.046/min), treated lean (0.032/min), control lean (0.026/min), and control obese (0.022/min). The obese mice showed less futile Cori cycle activity than the lean mice and ciglitazone had negligible effect on glucose recycling. The control obese mice incorporated more radiolabels in hepatic lipids, glycogen, and proteins than the control lean mice and ciglitazone further enhanced the incorporations. Ciglitazone also increased hepatic accumulations of radiolabels in the glycogen and lipid fractions in the lean littermates. Using lactate-14C as precursor, gluconeogenesis in vivo was measured in control and treated obese and lean mice. Ciglitazone significantly lowered the rate of conversion of lactate-14C to glucose-14C in the obese mice but not in the lean littermates.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00284462
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Islet innervation of nondiabetic and diabetic chinese hamsters I. Acetylcholinesterase histochemistry and norepinephrine fluorescence (1983)
    Springer
    Journal of neural transmission 56 (1983), S. 223-238 
    Details
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cholinergic and adrenergic innervation of pancreatic islets from age-and sex-matched nondiabetic (M subline) and diabetic (AC subline) Chinese hamsters was analyzed by acetylcholinesterase (AChE) histochemistry and norepinephrine fluorescence. The AChE activity was significantly diminished in islets of diabetic animals compared with that of nondiabetic controls. The reduction in cholinergic innervation displayed an inverse relationship with respect to nonfasting plasma glucose and ketone levels. On the basis of qualitative analysis, adrenergic activity also appeared to be depressed in islets of diabetic animals. These data suggest that autonomic control of islet function is altered in diabetic Chinese hamsters when plasma glucose and ketone levels are elevated and may exacerbate metabolic complications in this animal model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01243280
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    Paper (German National Licenses)
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