Advertisement
Review| Volume 14, ISSUE 3, P289-307, November 1971

Pathophysiologic responses to severe, chronic alloxan diabetes in arteriosclerotic and non-arteriosclerotic rats

  • B.C. Wexler
    Correspondence
    Address of the author: Dr. Bernard C. Wexler, Director, May Institute for Medical Research, 421 Ridgeway Avenue, Cincinnati, Ohio 45229 U.S.A.
    Footnotes
    Affiliations
    May Institute for Medical Research of the Jewish Hospital and Departments of Pathology and Medicine, University of Cincinnati, College of Medicine, Cincinnati, Ohio 45229 U.S.A.
    Search for articles by this author
  • Author Footnotes
    1 Dr. Wexler is supported by a Research Career Award Grant (HE-K3-1734), from the National Heart Institute, NIH, U.S. Public Health Service.
DOI:https://doi.org/10.1016/0021-9150(71)90059-1
Pathophysiologic responses to severe, chronic alloxan diabetes in arteriosclerotic and non-arteriosclerotic rats
Next ArticleThe role of phagocytosis in the development of atherosclerotic lesions in the rabbit
      This paper is only available as a PDF. To read, Please Download here.

      Abstract

      Repeatedly bred rats develop arteriosclerosis, hyperlipidemia, hyperglycemia and other degenerative changes, spontaneously. An injection of alloxan given to non-arteriosclerotic virgin and to arteriosclerotic and diabetic breeder rats caused severe ketosis, hyperglycemia, hyperlipidemia, marked alterations in serum enzymes and alterations in adrenal secretory activity. After two months, half of all of the diabetic animals were obese with little or no arteriosclerosis, the remaining half were emaciated with severe arteriosclerosis. This condition of obesity or emaciation persisted throughout the course of the experiment. This dichotomous response was ascribed to differences in beta cell recovery from alloxan. Treatment was deliberately withheld and the diabetes allowed to run unchecked until the animals began to die in great numbers, i.e., only 52 animals survived of a total of 2000. After 5 months of unrelenting diabetes, the severity of hyperglycemia lead become slightly reduced, adrenal function was definitely compromised, hyperlipidemia persisted except for cholesterol, serum transaminases (SGOT and SGPT) were greatly elevated but LDH was surprisingly reduced, and all subjects were hypercalcemic. All of the animals were blind and most of the obese subjects expired but the emaciated and arteriosclerotic animals survived. The formerly healthy virgin subjects had also developed blindness and advanced arteriosclerosis during the 5 months of unrelenting diabetes.

      Keywords

      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Atherosclerosis
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Register: Create an account
      Institutional Access: Sign in to ScienceDirect

      References

        • Bell E.T.
        A postmortem study of vascular disease in diabetes.
        Arch. Pathol. 1952; 53: 444
        • Clawson B.J.
        • Bell E.T.
        Incidence of fatal coronary disease in nondiabetic and diabetic persons.
        Arch. Pathol. 1949; 48: 105
        • Warren S.
        • LeCompte P.M.
        The Pathology of Diabetes Mellitus.
        3rd edition. Lea and Febiger, Philadelphia, Pa.,1952
        • Goldenberg G.
        • Alex M.
        • Blumenthal H.T.
        Sequelae of arteriosclerosis of aorta and coronary- arteries. Statistical study of diabetes mellitus.
        Diabetes. 1958; 7: 98
        • Knowles Jr, H.C.
        Prevalence and development of diabetes.
        in: Federation Proc.27. 1968: 945
        • Blumenthal H.T.
        The relation of microangiopathies to arteriosclerosis, with special reference to diabetes.
        Ann. N.Y. Acad. Sci. 1968; 149: 834
        • Camerini-Davlos R.A.
        • Caulfield J.B.
        • Rees S.G.
        • Lozano-Castaneda O.
        • Naldjian S.
        • Marble A.
        Vascular changes in pre-diabetes.
        in: Siperstein N.D. Colwell Sr, A.R. Meyer K. Small Blood Vessel Involvement in Diabetes Mellitus. A.I.B.S.,, Washington, D.C.,1964
        • Wexler B.C.
        • Fischer C.W.
        Hyperplasia of the islets of Langerhans in arteriosclerosic rats.
        Nature. 1963; 200: 33
        • Wexler B.C.
        • Fischer C.W.
        Abnormal glucose tolerance in repeatedly bred rats with arteriosclerosis.
        Nature. 1963; 200: 133
        • Wexler B.C.
        Arteriosclerosis of the renal artery in repeatedly bred male and female rats.
        Atherosclerosis. 1970; 11: 383
        • Wexler B.C.
        Spontaneous arteriosclerosis in repeatedly bred male and female rats.
        J. Atheroscler. Res. 1964; 4: 57
        • Wexler B.C.
        • True C.W.
        Carotid and cerebral arteriosclerosis in the rat.
        Circ. Res. 1963; 12: 659
        • Wexler B.C.
        Spontaneous coronary arteriosclerosis in repeatedly bred male and female rats.
        Circ. Res. 1964; 14: 32
        • Wexler B.C.
        Spontaneous arteriosclerosis of the mesenteric, renal and peripheral arteries of repeatedly bred rats.
        Circ. Res. 1964; 15: 485
        • Wexler B.C.
        • Kittinger G.W.
        Myocardial necrosis in rats: serum enzymes, adrenal steroid and histopathological alterations.
        Circ. Res. 1963; 13: 159
        • Wexler B.C.
        • Antony C.D.
        • Kittinger G.W.
        Serum lipoprotein and lipid changes in arteriosclerotic breeder rats.
        J. Atheroscler. Res. 1964; 4: 131
        • Wexler B.D.
        • Kittinger G.W.
        Spontaneous arteriosclerosis in male and female breeder rats: effects of a high fat diet and hyperadrenocorticism on repeatedly bred rats.
        J. Pathol. Bacteriol. 1967; 94: 231
        • Wexler B.C.
        Arteriosclerosis of the pancreas and changes in the islets of Langerhans of repeatedly bred rats.
        Brit. J. Exptl. Pathol. 1970; 51: 107
        • Wexler B.C.
        • Saroff J.
        • Judd J.T.
        Variations in response to severe alloxan diabetes in arteriosclerotic and non-arteriosclerotic rats.
        Diabetes. 1970; 19: 311
        • Wexler B.C.
        Histopathologic responses to severe alloxan diabetes in arteriosclerotic and non-arteriosclerotic rats.
        Diabetes. 1970; 19: 324
        • Guillemin R.
        • Clayton G.W.
        • Lipscombe H.S.
        • Smith J.D.
        Fluorometric measurement of rat plasma and adrenal corticosterone concentration.
        J. Lab. Clin. Med. 1959; 53: 830
        • Judd J.T.
        • Wexler B.C.
        The role of lactation and weaning in the pathogenesis of arteriosclerosis in female breeder rats.
        J. Atheroscler. Res. 1969; 10: 153
        • Wexler B.C.
        Spontaneous development of renal calculi in repeatedly bred rats.
        J. Urol. 1963; 89: 332
        • Wexler B.C.
        Histopathology of kidney stone formation in repeatedly bred rats.
        J. Urol. 1963; 90: 527
        • Wexler B.C.
        • Judd J.T.
        • Kittinger G.W.
        Changes in calcium, hydroxyproline and mucopolysaccharides in various aortic segments of arteriosclerotic breeder rats.
        J. Atheroscler. Res. 1961; 4: 397
        • Kraus S.D.
        Impairment of the pituitary-adrenal response to acute stress in alloxan diabetes.
        Acta Endocrinol. 1967; 54: 328
        • Kraus S.D.
        • Cohen K.A.
        Corticosterone and ACTH in alloxan diabetic rats.
        in: Program 52nd Meeting of Endocrine Society. June, 1970 (St. Louis, Mo.)
        • Vargas L.
        • Friederici H.H.K.
        • Maibenco H.C.
        Cortical sponge kidneys induced in rats by alloxan.
        Diabetes. 1970; 19: 33

      Article info

      Publication history

      Received: December 24, 1970

      Footnotes

      ☆This work was supported, in part, by grants from the Southwestern Ohio Heart Association, the National Heart Institute (HE-6315) and by a General Research Support Grant (RR 5633) from the National Institutes of Health.

      Identification

      DOI: https://doi.org/10.1016/0021-9150(71)90059-1

      Copyright

      © 1971 Published by Elsevier Inc.

      ScienceDirect

      Access this article on ScienceDirect
      We use cookies to help provide and enhance our service and tailor content. To update your cookie settings, please visit the for this site.
      Copyright © 2023 Elsevier Inc. except certain content provided by third parties. The content on this site is intended for healthcare professionals.


      RELX