Abstract

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.