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Clinical Science (1998) 95, (735–744) (Printed in Great Britain)

Gastrectomy osteopenia in the rat: the role of vitamin B12 deficiency and the type of reconstruction of the digestive tract

A. WOJTYCZKA*1, B. BERGÉ*, G. RÜMENAPF*†, P. O. SCHWILLE*, P. BALLANTI‡, M. SCHREIBER*†, W. FRIES* and W. HOHENBERGER†

*Division of Experimental Surgery and Endocrine Research Laboratory, University of Erlangen, D-91023 Erlangen, Germany, †Department of Surgery, University of Erlangen, D-91023 Erlangen, Germany, and ‡Department of Experimental Medicine and Pathology, La Sapienza, University of Rome, Italy

Abbreviations: GX, gastrectomy; PTH, parathyroid hormone.

Correspondence: Dr P. O. Schwille.

¹ On leave from the Department of Gastrointestinal Surgery, Silesian University Medical School, Katowice, Poland.

1. The mechanisms underlying gastrectomy osteopenia are not yet clear. The gastrectomy-associated cobalamin (vitamin B₁₂) deficiency may favour osteopenia and skeletal fractures. Also, the exclusion of the duodenum from the food passage may contribute to gastrectomy osteopenia. To investigate this, rats were gastrectomized and the passage of nutrients restored either with the duodenum excluded (Roux Y) or included (Longmire). Sham-operated rats served as controls. In half of the rats in each gastrectomy group the serum B₁₂ levels were normalized by parenteral administration of B₁₂.

2. Four months post operation, both gastrectomy groups showed a similar degree of osteopenia. There was normal bone mineralization; serum levels of parathyroid hormone were normal, but decreased for 25-hydroxyvitamin D, and elevated for 1,25-dihydroxyvitamin D; in urine there was decreased pH and excessive hyperphosphaturia.

3 B₁₂ therapy had no influence on any of the essential bone and mineral metabolic parameters.

4. We conclude that osteopenia in the gastrectomized rat (i) is not due to B₁₂ or folic acid deficiency, calcium deficiency or secondary hyperparathyroidism; (ii) is independent of the type of anatomic reconstruction of the digestive tract; (iii) appears to be related to disturbed vitamin D, phosphorus and acid–base metabolism.

Received 8 April 1998/7 July 1998; accepted 9 July 1998

The Biochemical Society and the Medical Research Society © 1998