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Caffeine Inhibits Fluid Secretion by Interlobular Ducts From Guinea Pig Pancreas

Mochimaru, Yuka MA; Yamamoto, Akiko MD, PhD; Nakakuki, Miyuki BS; Yamaguchi, Makoto ME; Taniguchi, Ituka MA; Ishiguro, Hiroshi MD, PhD

doi: 10.1097/MPA.0000000000000782
Original Articles

Objectives Caffeine is contained in coffee, tea, and numerous beverages and foods. We examined the direct effects of caffeine on the physiological function of pancreatic duct cells by using interlobular duct segments isolated from guinea pig pancreas.

Methods The rate of fluid secretion was continuously measured by monitoring the luminal volume of isolated duct segments. Changes in intracellular Ca2+ concentration ([Ca2+]i) were estimated by microfluorometry in ducts loaded with Fura-2.

Results Both secretin-stimulated and acetylcholine (ACh)-stimulated fluid secretions were substantially and reversibly inhibited by relatively low concentrations of caffeine as low as 0.03 mM relevant to blood levels after ingestion of caffeine-containing beverages. Caffeine inhibited ACh-induced elevation of [Ca2+]i and secretin-induced fluctuation of [Ca2+]i. Caffeine abolished thapsigargin-induced intracellular Ca2+ release but did not affect the entry of extracellular Ca2+. Caffeine (0.05 mM) abolished ethanol (1 mM)-induced fluid hypersecretion in secretin-stimulated pancreatic duct.

Conclusions Low concentrations of caffeine directly inhibit pancreatic ductal fluid secretion stimulated by secretin or ACh and also ethanol-induced fluid hypersecretion. The inhibition by caffeine seems to be mediated by the blockade of intracellular Ca2+ mobilization. Daily intake of caffeine may reduce the volume of pancreatic juice secretion.

From the Department of Human Nutrition, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Received for publication November 19, 2015; accepted October 19, 2016.

Address correspondence to: Hiroshi Ishiguro, MD, PhD, Department of Human Nutrition, Nagoya University Graduate School of Medicine, Research Center of Health, Physical Fitness, and Sports, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464–8601, Japan (e-mail: ishiguro@htc.nagoya-u.ac.jp).

This study was supported by grants from the Japan Society for the Promotion of Science and the Research Committee of Intractable Pancreatic Diseases (principal investigator: Yoshifumi Takeyama) provided by the Ministry of Health, Labour, and Welfare of Japan.

The authors declare no conflict of interest.

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