PT  - JOURNAL ARTICLE
AU  - Sutep Gonlachanvit
AU  - Yen Hsueh Chen
AU  - William L. Hasler
AU  - Wei Ming Sun
AU  - Chung Owyang
TI  - Ginger Reduces Hyperglycemia-Evoked Gastric Dysrhythmias in Healthy Humans: Possible Role of Endogenous Prostaglandins
AID  - 10.1124/jpet.103.053421
DP  - 2003 Dec 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 1098--1103
VI  - 307
IP  - 3
4099  - http://jpet.aspetjournals.org/content/307/3/1098.short
4100  - http://jpet.aspetjournals.org/content/307/3/1098.full
SO  - J Pharmacol Exp Ther2003 Dec 01; 307
AB  - Acute hyperglycemia evokes gastric slow wave dysrhythmias via endogenous prostaglandin generation. Ginger exhibits slow wave antiarrhythmic effects in other models, but its actions on hyperglycemia-evoked gastric dysrhythmias are unexplored. We hypothesized that ginger prevents disruption of slow wave rhythm by acute hyperglycemia via inhibition of prostaglandin production but not its actions. Twenty-two healthy humans underwent fasting electrogastrography during hyperglycemic clamping to 250 to 290 mg/dl after double-blind placebo or ginger root (1 g). Responses were compared with the prostaglandin E1 analog misoprostol (400 μg). Dominant frequencies (DF) and the percentage of recording times in the bradygastric [0.5–2 cycles/min (cpm)], normal (2–4 cpm), and tachygastric (4–9 cpm) frequency ranges were analyzed. After placebo, hyperglycemia reduced normal 2 to 4 cpm activity from 94.4 ± 2.6 to 66.0 ± 10.4%, increased the DF from 2.96 ± 0.04 to 4.09 ± 0.45 cpm, and increased tachygastria from 2.0 ± 1.4 to 29.3 ± 10.7% (P < 0.05). Hyperglycemia effects on normal activity (77.3 ± 8.3%), DF (3.46 ± 0.37 cpm), and tachygastria (15.6 ± 8.6%) were significantly reduced by ginger (P < 0.05). Misoprostol evoked decreases in normal activity from 95.4 ± 2.0 to 81.7 ± 3.0% and increases in tachygastria from 3.1 ± 1.6 to 11.2 ± 2.4% (P < 0.05). However, ginger did not correct these abnormalities versus placebo (P = N.S.). In conclusion, acute hyperglycemia evokes gastric slow wave dysrhythmias that are prevented by ginger root. Conversely, the compound has no effect on dysrhythmias elicited by a prostaglandin E1 analog, indicating that ginger likely acts to blunt production of prostaglandins rather than inhibiting their action. These findings suggest novel mechanisms for the traditional Chinese herbal remedy ginger. The American Society for Pharmacology and Experimental Therapeutics