Download PDF
Horm Metab Res 1978; 10(5): 389-392
DOI: 10.1055/s-0028-1093398
Originals

© Georg Thieme Verlag KG Stuttgart · New York

Effects of Pinealectomy and of Sham-Pinealectomy on Blood Glucose Levels in the Alloxan-Diabetic Rat[*]

K. C. Gorray [**] , W. B. Quay [***]
  • Endocrinology-Reproductive Physiology Program, and Neuroendocrinology Section, Waisman Center on Mental Retardation and Human Development, University of Wisconsin, Madison, Wisconsin, USA
Further Information

Publication History

Publication Date:
23 December 2008 (online)

Also available at
  PDF Download  Permissions and Reprints

Abstract

Alloxan-diabetic male rats were used to test effects of pinealectomy (PX) and of sham-pinealectomy (SPX) on blood glucose levels at mid-dark in the daily light-dark (LD 12: 12) cycle. Animals received a diabetogenic dose of alloxan 10 days postoperatively. Blood glucose was measured on days -1, 1, 2, 3, 4, 5, 7, 10 and 15 after 8-hour fasts.

Pinealectomized (PX) and non-operated (C) animals were equivalent in their hyperglycemia following alloxan. SPX animals contrastingly showed significantly less response to alloxan than did animals of the other two groups. This difference of the SPX animals was in terms of lower hyperglycemia, better maintenance of body weight and of survival.

It is concluded that intracranial surgery alone (SPX) and without visible brain damage can affect mechanisms of glucose homeostasis, and that at least in some circumstances such a surgical effect is not only different from effects of surgical pinealectomy (PX), but is also probably not pineal-dependent.

Key words

Alloxan Diabetes - Blood Glucose - Pinealectomy - Surgical Effects

1 This work was supported in part by a fellowship (K.C.G.) from the University of Wisconsin, Madison, School of Graduate Studies, and research grants (W.B.Q.) from the National Institute of Mental Health (MH-25091), the National Institute of Health (HD-03352, HD-10263, 5-T01-HD-00104-10), USPHS, the Ford Foundation (#630-0505 B, C) and the National Science Foundation (PCM 76-09953).

1 This work was supported in part by a fellowship (K.C.G.) from the University of Wisconsin, Madison, School of Graduate Studies, and research grants (W.B.Q.) from the National Institute of Mental Health (MH-25091), the National Institute of Health (HD-03352, HD-10263, 5-T01-HD-00104-10), USPHS, the Ford Foundation (#630-0505 B, C) and the National Science Foundation (PCM 76-09953).

2 Present address: Department of Medicine, Center for Health Sciences, University of Wisconsin School of Medicine, Madison, Wisconsin 53706.

3 Present address: Neuroendocrine Laboratory, Department of Anatomy, University of Texas Medical Branch, Galveston, Texas 77550.

      >