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氫水有助於減重之研究 (通過誘導肝臟FGF21促進能量代謝)
氫氣通過誘導肝臟FGF21促進能量代謝治療肥胖
日本醫科大學太田成男教授小組又發關於氫氣治療疾病的重要文章，2007年他們是國際上首先證明氫氣通過選擇性抗氧化治療中風，該實驗室是日本醫科大學老年病研究所，過去主要從事線粒體與氧化損傷方面的研究，研究的疾病主要包括腦血管疾病、代謝性疾病、神經退行性疾病如老年性癡呆、巴金森病等。最近幾年他們圍繞氫氣對上述疾病的治療，開展了大量非常深入的系統研究。
本研究是發現氫氣具有減肥作用，也是非常吸引人的研究課題，2年前他們發現這個效應後，就已經申請了氫氣具有減肥作用的國際專利。
本研究發表在國際著名雜誌Obesity , (3 February 2011)
| doi:10.1038/oby.2011.6，研究的內容非常豐富，首先他們研究發現氫氣水可以促進肝臟糖原的聚集（保肝藥物都這樣，將來研究肝臟保護方面的研究者可以使用這個指標），採用糖原溶液能保持氫氣的實驗初步解釋為什麼短時間給氫氣對許多疾病具有很強的治療效果。然後他們用缺乏瘦素受體的db/db小鼠，證明氫水可以治療二型糖尿病，對正常高脂飲食引起動物脂肪肝也具有顯著治療效果，長期飲用氫水可以在不減少飲食飲水量的條件下降低動物體重，減少體脂肪，也就是說具有減肥作用。同時動物的血糖、胰島素和甘油三脂都顯著下降，這些效果與限制飲食的效果類似。
為了研究氫氣為什麼具有這些令人驚奇的減肥效果，他們採用PCR技術，發現氫氣能提高肝臟的一種重要激素成纖維細胞生長因數21（FGF21）的水準，FGF21的作用是促進脂肪酸和葡萄糖的利用，他們還採用氧消耗對氫氣促進代謝的效應進行了驗證。研究提示，氫氣可能是對治療糖尿病、代謝綜合征和肥胖具有潛在的價值。這個研究也再次深化了氫氣生物學效應的分子機制，對解釋為什麼氫氣能治療動脈硬化、中風和神經退行性疾病有重要參考價值。在氫氣生物學領域將是一篇具有重要影響的經典文獻。
關於FGF21的延伸閱讀：在動物實驗中，FGF21已被證實能夠降低血糖、血脂，抑制胰高血糖素分泌，促進胰島素分泌，提高胰島素敏感性，改善胰腺β細胞功能及存活率，調節血液迴圈中脂肪細胞因數。還有研究表明，FGF21能降低血漿白介素-8、C反應蛋白、纖溶酶原啟動劑抑制因數-1水準，升高脂聯素水準。此外，FGF21還可通過血腦屏障。為此，有人認為FGF21在將來有望成為一種新型降糖藥。
本文氫水製備之方式是應用高壓灌注氫氣 (0.4 MPa) ，密封保存於常溫常壓下的鋁箔包中密封
In brief, H2 was dissolved in water under high pressure (0.4 MPa) to a supersaturated level and the saturated H2 -water was stored under atmospheric pressure in an aluminum bag with no dead volume
原文章出處
Molecular Hydrogen Improves Obesity and Diabetes by Inducing Hepatic FGF21 and Stimulating Energy Metabolism in db/db Mice
Naomi Kamimura, Kiyomi Nishimaki, Ikuroh Ohsawa and Shigeo Ohta
Recent extensive studies have revealed that molecular hydrogen (H2) has great potential for improving oxidative stress-related diseases by inhaling H2 gas, injecting saline with dissolved H2, or drinking water with dissolved H2 (H2-water); however, little is known about the dynamic movement of H2 in a body. First, we show that hepatic glycogen accumulates H2 after oral administration of H2-water, explaining why consumption of even a small amount of H2 over a short span time efficiently improves various disease models. This finding was supported by an in vitro experiment in which glycogen solution maintained H2. Next, we examined the benefit of ad libitum drinking H2-water to type 2 diabetes using db/db obesity model mice lacking the functional leptin receptor. Drinking H2-water reduced hepatic oxidative stress, and significantly alleviated fatty liver in db/db mice as well as high fat-diet-induced fatty liver in wild-type mice. Long-term drinking H2-water significantly controlled fat and body weights, despite no increase in consumption of diet and water. Moreover, drinking H2-water decreased levels of plasma glucose, insulin, and triglyceride, the effect of which on hyperglycemia was similar to diet restriction. To examine how drinking H2-water improves obesity and metabolic parameters at the molecular level, we examined gene-expression profiles, and found enhanced expression of a hepatic hormone, fibroblast growth factor 21 (FGF21), which functions to enhance fatty acid and glucose expenditure. Indeed, H2 stimulated energy metabolism as measured by oxygen consumption. The present results suggest the potential benefit of H2 in improving obesity, diabetes, and metabolic syndrome.
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