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G. C. BOND, J. N. PASLEY, T. I. KOIKE and L. LLERENA

Department of Physiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72201, U.S.A.

(Received 27 April 1976)

The administration of various prolactin preparations to mammals has been shown to decrease urine flow (Lockett & Nail, 1965; Horrobin, Lloyd, Lipton, Burstyn, Durkin & Muiruri, 1971) and suppress diuresis induced by expansion of the extracellular fluid volume with saline (Lucci, Bengele & Solomon, 1975). It was assumed in these studies that the antidiuresis was due to prolactin. Antidiuretic hormone (ADH), however, may be present in certain ovine extracts from the pituitary which also could lead to a decrease in urine flow and suppression of diuresis (Rabkin, Swann, Shapiro & Isaacson, 1974). Consequently, we examined the possibility that ADH was present in an ovine prolactin preparation (NIH-P-S10) in quantities sufficient to cause antidiuresis.

Experiments were performed on male, Sprague–Dawley rats anaesthetized with pentobarbitone. The rats were placed in the ventral position on

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W Yin, D Liao, M Kusunoki, S Xi, K Tsutsumi, Z Wang, X Lian, T Koike, J Fan, Y Yang and C Tang

The synthetic compound NO-1886 (ibrolipim) is a lipoprotein lipase activator that has been proven to be highly effective in lowering plasma triglycerides. Recently, we found that NO-1886 also reduced plasma free fatty acids and glucose in high-fat/high-sucrose diet-induced diabetic rabbits. In the current study, we investigated the effects of NO-1886 treatment on ectopic lipid deposition and the islet pathology in miniature swine fed a high-fat/high-sucrose diet. Our results showed that feeding this diet to miniature swine caused insulin resistance, increased lipid deposition in non-adipose tissue, such as in the heart, skeletal muscle, liver and pancreas, and also caused pancreatic beta cell damage. However, supplementing 1% NO-1886 (200 mg/kg per day) into the high-fat/high-sucrose diet decreased ectopic lipid deposition, improved insulin resistance, and alleviated the beta cell damage. These results suggest that improvement of lipid disorder, non-adipose tissue steatosis and insulin resistance may be very important for the protection of beta cell damage. Therefore, NO-1886 is potentially beneficial for the treatment of insulin-resistance syndrome.