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Pancreastatin-Like Immunoreactivity in Urine

Biochemistry (K.T., Y.M.), School of Medicine, Fukuoka University Fukuoka, Japan;
First Laboratory of Clinical Physiology (K.M.), Tokyo Metropolitan Institute of Gerontology Tokyo, Japan;
National Kyushu Cancer Center (H.S., A. F.) Fukuoka, Japan;
Faculty of Pharmaceutical Sciences (S. F.), Kyoto University Kyoto, Japan

Address correspondence and requests for reprints to: Dr. K. Tateishi, The First Department of Biochemistry, School of Medicine, Fukuoka University, 7-45-1, Nanakuma, Jonan-ku, Fukuoka 814-01, Japan.

The concentration and molecular form of pancreastatin-like immunoreactivity (PST-LI) in urine of normal subjects and patients with noninsulin-dependent diabetes mellitus or chronic renal failure were examined. PST-LI output (mean ± SEM) in urine of normal subjects was 74.6 ± 8.5 pmol/day and 87.1 ± 11.7 pmol/g creatinine. That in patients with noninsulin-dependent diabetes mellitus was 78.1 ± 9.0 (SEM) pmol/day and 85.6 ± 9.0 pmol/g creatinine and was not significantly different from that in normal subjects. Gel filtration analysis showed that PST-LI molecules excreted in urine of these two groups were smaller than human pancreastatin (43–52) (hPST-10) of C-terminal fragment. The PST-LI molecular forms were deduced to be nonbioactive from the result that hPST-10 did not inhibit pancreatic exocrine secretion. PST-LI excretion in patients with chronic renal failure was 258.5 ± 62.9 pmol/day and 713.2 ± 219.6 pmol/g creatinine. A molecular form corresponding to hPST-52 and a larger form eluted in the high mol wt region (mol wt 15 K) were detected by gel filtration of urine from these patients, indicating that PST-LI is excreted in urine without degradation in patients with chronic renal failure. These results support the suggestion that the kidney may play an important role in PST degradation or metabolism.

Received January 29, 1990.