A genetically diabetic model "KK-CAy mice" for a pharmacological assay.

Kimura, Masayasu; Suzuki, Jun; Amemiya, Kouji

doi:10.1507/endocrj1954.26.185

Cited by 33 publications

(20 citation statements)

References 7 publications

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“…The male KK-CAy mouse has a genetically predisposed syndrome similar to human type II diabetes mellitus (NIDDM) and includes hyperglycemia, hyperinsulinemia, obesity, and insulin resistance (Kimura et al, 1979). In the diabetic KK-CAy mouse and alloxan-induced diabetic mouse, neuromuscular blocking drug succinylcholine (SuCh) showed enhanced inhibitory sensitivity for acetylcholine (ACh) receptors at the neuromuscular synapse of gastrocnemius muscles (Kimura et al, 1986 c;.…”

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confidence: 99%

Diabetic State-Induced Activation of Calcium-Activated Neutral Proteinase in Mouse Skeletal Muscle.

et al. 1989

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The effect of a diabetic state in the diabetic KK-CAY mouse on calcium activated neutral proteinase (CANP) of hind-limb skeletal muscles was investigated. In the diabetic state, there was an increased sensitivity to activation of CANP by calcium (Ca). In addition, there was an enhancement of maximal activity of the enzyme. The effect was induced by secondary modification of the diabetic state, but not genetical factors. Several lines of evidence suggest that the CANP is responsible for 92 K dalton protein in diabetic skeletal muscles. Among the evidence are the following:a) The 92 K band in the diabetic muscles was lower than in the prediabetic mouse and restored by the addition of 2mM EDTA and 2mM EGTA, b) The band was reduced by increasing the Ca content and neutral pH in the non-diabetic normal muscles. c) E-64-C, a CANP inhibitor, restored the 92K component reduced by the diabetic state. Since the band in denervated muscles was not changed by the Ca chelating agents, the reduction of the band in the diabetic muscles is related with musclotrophic factors, not diabetic neuropathy.These results suggest that diabetic amyotrophy may be regarded as a phenomenon linked to an increase in intracellular Ca ions and an increase in CANP activity.

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Diabetic State-Induced Activation of Calcium-Activated Neutral Proteinase in Mouse Skeletal Muscle.

et al. 1989

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“…It has been shown that insulin sensitivity is depressed in KK-CA y mice (Kimura et al, 1979). Subsequent detailed experiments showed that the sensitivity in diabetic KKCAy mice was four times less than in control non-diabetic KK mice (unpublished data).…”

Section: Discussionmentioning

confidence: 89%

“…As previously reported (Kimura et al, 1979), KK-CAY mice in which AY gene has been transferred with the color (C) gene into the KK background are very useful diabetic models since they are obese, hyperinsulinemic, and severely hyperglycemic. Islet hy- …”

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confidence: 84%

“…The genetically diabetic KK-CAY mice (male, 8-20weeks old) used came from the closed colony in our laboratory (Kimura et al, 1979 Measurement of DNA content in the pouch granuloma, blood glucose, and insulin concentration Deoxyribonucleic acid (DNA) was extracted from the pouch granuloma by the method of Schneider (1946). Its content was determined according to the modified method of Burton (1956).…”

Section: Animalsmentioning

confidence: 99%

“…Its content was determined according to the modified method of Burton (1956). Blood glucose levels were measured with a Beckman Glucose Analyzer, and the insulin in the plasma and the exudate was assayed by the radioimmunological method (Kimura et al, 1979).…”

Section: Animalsmentioning

confidence: 99%

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Insulin Resistance of Adjuvant-Induced Granuloma Pouch Formation in Genetically Diabetic KK-CA<SUP>y</SUP> Mice

et al. 1987

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The characteristics of adjuvant-induced pouch granuloma in genetically diabetic KK-CAy mice with hyperinsulinemia were investigated. Both the dose-response relationship and the time-course experiments showed that the wet weight of pouch granuloma in diabetic KK-CAy mice was lower than in ddY normal mice. Insulin treatment enhanced granuloma formation in KKCAy mice, and it restored the suppressed DNA content in the granuloma tissue to the level in ddY mice. Although the DNA content was dosedependently increased by insulin, the ratio of DNA content to granuloma weight was constant. In severely diabetic mice, the granuloma weight was not different from that in normoglycemic mice, despite significantly higher blood insulin levels and greater body weight. Insulin stimulated granuloma formation in severely diabetic KK-CAy mice only when higher doses (1mg/kg) were given. This evidence suggests that suppression of granuloma formation in diabetic KK-CAy mice is due to insulin resistance and that restoration requires pharmacological doses of insulin.

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The antihyperglycaemic blend effect of traditional Chinese medicine Byakko-ka-ninjin-to on alloxan and diabetic KK-CAy mice

et al. 1999

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A genetically diabetic model "KK-CAy mice" for a pharmacological assay.

Cited by 33 publications

References 7 publications

Diabetic State-Induced Activation of Calcium-Activated Neutral Proteinase in Mouse Skeletal Muscle.

Diabetic State-Induced Activation of Calcium-Activated Neutral Proteinase in Mouse Skeletal Muscle.

Insulin Resistance of Adjuvant-Induced Granuloma Pouch Formation in Genetically Diabetic KK-CA<SUP>y</SUP> Mice

The antihyperglycaemic blend effect of traditional Chinese medicine Byakko-ka-ninjin-to on alloxan and diabetic KK-CAy mice

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