Induction of Overt Diabetes in KK Mice by Dietary Means
KK mice fed on semisynthetic diets with a usual composition developed marked obesity and diabetic symptoms in comparison with those kept on laboratory chow. The observed changes included obesity, fatty liver, glucosuria, hyperglycemia and degranulation of pancreatic B cells. These changes became mor...
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Published in | Endocrinologia Japonica Vol. 17; no. 6; pp. 477 - 488 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Japan
The Japan Endocrine Society
01.01.1970
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Abstract | KK mice fed on semisynthetic diets with a usual composition developed marked obesity and diabetic symptoms in comparison with those kept on laboratory chow. The observed changes included obesity, fatty liver, glucosuria, hyperglycemia and degranulation of pancreatic B cells. These changes became more prominent with prolonged period of feedig up to 24 weeks. Among them, fatty liver and obesity were also induced in control ICR mice upon feeding semisynthetic diets but the developments were limited in moderate degree and no diabetic symptom developed. These results indicate that the different response to diets in both mice can be attributed to genetic factors. |
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AbstractList | KK mice fed on semisynthetic diets with a usual composition developed marked obesity and diabetic symptoms in comparison with those kept on laboratory chow. The observed changes included obesity, fatty liver, glucosuria, hyperglycemia and degranulation of pancreatic B cells. These changes became more prominent with prolonged period of feedig up to 24 weeks. Among them, fatty liver and obesity were also induced in control ICR mice upon feeding semisynthetic diets but the developments were limited in moderate degree and no diabetic symptom developed. These results indicate that the different response to diets in both mice can be attributed to genetic factors. |
Author | SHINO, AKIO MATSUO, TAKAO IWATSUKA, HISASHI SUZUOKI, ZIRO |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/4931786$$D View this record in MEDLINE/PubMed |
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References | Gerson, T.(1960). Biochem. J., 77, 446. Iwatsuka, H., A. Shino and Z. Suzuoki (1970b). Endocrinol. Japon., 17, 23. Iwatsuka, H., T. Matsuo, A. Shino and Z. Suzuoki (1970a). J. Takeda Res. Lob., 29, 685. Dulin, W. E. and G. C. Gerritsen (1967). Proc. 6th. Congr. Diabetes Fed., (Stockholm). Hackel, D. B., H. E. Lebovitz, L. A. Frohman, E. Miki and K. Schmidt-Nielsen (1967). Metabolism, 16, 1133. Huggett, A. St. G. and D. A. Nixon (1957). Lancet, ii, 368. Batt, R. and P. Mialhe (1966). Nature, 212, 289. Haines, H., D. B. Hackel and K. Schmidt-Nielsen (1965). Am. J. Physiol., 208, 297. Gleason, R. E., V. Lauris and J. S. Soeldner (1967). Diabetologia, 3, 175. Nakamura, M.(1962). Proc. Japan Acad., 38, 348. Hellman, B.(1965). Ann. N. Y. Acad. Sci., 131, 541. Miki, E., A. A. Like, J. Steinke and L. S. Soeldner (1967). Diabetologia, 3, 135. Petersson, B. and B. Hellman (1962). Metabolism, 11, 342. Tsuchida, I.(1966). J. Japan Diabetic Soc., 9, 67.(In Japanese). |
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SubjectTerms | Adipose Tissue Animals Body Weight Cholesterol - analysis Diabetes Mellitus - etiology Diabetes Mellitus - genetics Diabetes Mellitus - pathology Diet Epididymis Fatty Acids - analysis Fatty Liver - etiology Glucose Tolerance Test Glycosuria - etiology Hyperglycemia - etiology Islets of Langerhans - pathology Lipids - analysis Liver - analysis Male Mice Obesity - etiology Organ Size |
Title | Induction of Overt Diabetes in KK Mice by Dietary Means |
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