Parker Barbara A, Doran Selena, Wishart Judith, Horowitz Michael, Chapman Ian M
Department of Medicine, University of Adelaide, Royal Adelaide Hospital, North Terrace, Adelaide, South Australia, Australia.
Clin Endocrinol (Oxf). 2005 May;62(5):539-46. doi: 10.1111/j.1365-2265.2005.02254.x.
Ghrelin is a peptide hormone secreted primarily from the gastric mucosa. It plays a role in energy balance by stimulating appetite, thereby increasing food intake and enhancing weight gain and fat mass deposition. Plasma ghrelin concentrations increase with fasting and are suppressed by nutrient intake. The aim of this study was to examine in humans the relative contributions of small intestinal and gastric nutrient exposure to postprandial suppression of ghrelin, to determine whether gastric exposure is necessary for ghrelin suppression.
Twelve healthy older (age range 65-85 years) men (n = 7) and women (n = 5) were studied.
On three separate days, equivolaemic (315 ml) intragastric (IG) and intraduodenal (ID) carbohydrate solutions (both 300 kcal) or intragastric water (control) were infused over 150 min.
Food intake was quantified at a buffet meal offered immediately following each 150-min infusion. Blood ghrelin, cholecystokinin and glucose concentrations were measured.
There was a 25% suppression of mean plasma ghrelin concentrations following ID glucose (ID 2016 vs. control 2686 ng/l, P < 0.0001) and a 19% suppression following IG glucose (IG 2181 vs. control 2686 ng/l, P < 0.0001), with ghrelin concentrations slightly (7.6%) and nonsignificantly lower after ID than after IG glucose infusions (P = 0.2). There was no difference between the treatments for the amount of food consumed at the buffet meal (P = 0.88).
Although the primary source of ghrelin is the gastric mucosa, these results suggest that small intestinal nutrient exposure is sufficient for food-induced plasma ghrelin suppression in humans, and that gastric nutrient exposure is not necessary for suppression.
胃饥饿素是一种主要由胃黏膜分泌的肽类激素。它通过刺激食欲在能量平衡中发挥作用,从而增加食物摄入量、促进体重增加和脂肪堆积。血浆胃饥饿素浓度随禁食而升高,并因营养物质摄入而受到抑制。本研究的目的是在人体中检验小肠和胃对营养物质的接触在餐后对胃饥饿素抑制作用中的相对贡献,以确定胃接触对于胃饥饿素抑制是否必要。
研究了12名健康的老年男性(7名)和女性(5名),年龄范围为65至85岁。
在三个不同的日子里,在150分钟内输注等容量(315毫升)的胃内(IG)和十二指肠内(ID)碳水化合物溶液(均为300千卡)或胃内水(对照)。
在每次150分钟输注后立即提供的自助餐中对食物摄入量进行量化。测量血液中的胃饥饿素、胆囊收缩素和葡萄糖浓度。
十二指肠内输注葡萄糖后平均血浆胃饥饿素浓度降低了25%(十二指肠内2016 vs. 对照2686纳克/升,P < 0.0001),胃内输注葡萄糖后降低了19%(胃内2181 vs. 对照2686纳克/升,P < 0.0001),十二指肠内输注葡萄糖后胃饥饿素浓度略低(7.6%)但无显著差异(P = 0.2)。自助餐中所消耗食物量在各治疗组之间无差异(P = 0.88)。
虽然胃饥饿素的主要来源是胃黏膜,但这些结果表明,在人体中,小肠对营养物质的接触足以使食物引起血浆胃饥饿素的抑制,且胃对营养物质的接触对于抑制并非必要。