奥利司他项目简介
2016年山东省重点建设项目名单
2016年省重点建设项目名单1济青岛高铁（正线307公里）2济青高速改扩建项目（高速公路309公里）3潍城至日照公路（高速公路154公里）东阿至聊城鲁冀界公路（高速公路86公里）泰安至东阿公路（高速公路74公里）滨莱高速公路淄博西至莱芜段扩建项目（高速公路73公里）龙口至青岛公路龙口至莱西（沈海）段（高速公路67公里）青岛新机场（2条3600米跑道）济南市轨道交通R3线一期工程（全长19.9公公里）滨港铁路沾化至滨州港段（新建正线65.3公里，改建1.7公里）中南部铁路通道郭家沟至大石家地方铁路线项目（正线14.2公里）日照机场至沈海高速连接线项目（全长3.9公里）烟台港西港区通用泊位、航道项目（1个10万吨级、2个7万吨级通用泊位，30万吨级航道35公里）日照港岚山港区原油码头二期工程（1个30万吨级原油泊位）东营港防波堤项目（东营港区南防波堤8613米，广利港区防波堤5065米）新万福河复航工程（全长61.3公里）京杭运河万年闸复线船闸项目（2千吨级二线船闸）榆横-潍坊1000千伏特高压交流输变电工程山东段（新建潍坊1000千伏变电站，扩建济南1000千伏变电站，石家庄-济南-潍坊1000千伏线路）内蒙古上海庙-山东临沂+-800千伏特高压交流输变电工程山东段（新建临沂800千伏换流站，上海庙-临沂800千伏线路）山东省500千伏输变电工程（新建智圣、峄城、东阿、惠民、儒林、临朐、垦东500千伏变电站）山东省2015年第一批专项农网改造升级工程（改造110千伏变电站29座，线路93公里；改造35千伏变电站40座，线路570公里；改造10千伏线路1.2万公里）文登抽水蓄能电站项目（总装机容量180万千瓦）枣庄庄里水库项目（总库容1.3亿立方米）聊城东昌府区南水北调续建配套项目（年供水量5183万立方米）威海市南海新区香水河挡潮闸项目（挡潮闸总宽463米）淄博市孝妇河黄土崖段综合整治项目（整治河道6.7公里）桓台县生态水系修复提升工程（修复提升水系258公里、水域面积208万平方米、湿地面积232万平方米）国家海洋设备质量监督检验中心项目（总建筑面积6.2万平方米）青岛环球金融中心项目（总建筑面积30.7万平方米）烟台蓝色智谷项目（总建筑面积29.8万平方米）淄博高新区医药创新中心建设项目（总建筑面积16.5万平方米）青岛船舶与海洋工程装备创新科技园项目（总建筑面积9.3万平方米）中兴（山东）智慧城市产业园一期项目（总建筑面积25.7万平方米）济南创新谷加速器建大合新产业基地项目（总建筑面积44.1万平方米）鑫茂齐鲁科技城二期项目（总建筑面积57万平方米）中关村海淀园齐河科技城一期项目（总建筑面积35.8万平方米）山东维度孵化器科技创新产业园项目（总建筑面积43.2万平方米）烟台国际节能环保科技园项目（总建筑面积14万平方米）泰安市联合绿色建材产业集聚区建设项目（总建筑面49.5万平方米）曹县大集镇淘宝产业园项目总建筑面积19.9万平方米莱芜颐高电子商务产业园项目总建筑面积24.6万平方米昌邑华海贸易广场“互联网+”项目（总建筑面积16.4万平方米）鄄城县城乡信息化产业园项目总建筑面积34.4万平方米东营综合保税区项目总建筑面积9.4万平方米菏泽铁路物流中心项目总建筑面积16.6万平方米，铁路专用线4.6公里淄博远成齐鲁综合物流港项目总建筑面积127.8万平方米菏泽传化智能公路港项目总建筑面积47.5万平方米中国兰陵三农物资批发城项目总建筑面积16.3万平方米银座国际汽车中心项目总建筑面积29万平方米潍柴动力全球配件分销中心项目总建筑面积11.9万平方米泉林循环经济产业园自动化立体仓储物流中心项目总建筑面积4.5万平方米潍坊申易现代物流项目总建筑面积9.1万平方米新易泰现代商贸物流园项目总建筑面积21.7万平方米山东设计创意产业园项目总建筑面积35万平方米山东银光文化创意产业基地项目总建筑面积7.9万平方米印象济南文化创意建设项目总建筑面积5.8万平方米博兴龙华文化园一期工程总建筑面积19.5万平方米菏泽鲁西南民俗文化记忆建设项目总建筑面积13.2万平方米枣庄市抱犊崮-熊耳山风景区5A级景区提升工程总建筑面积5.8万平方米青岛万达东方影都一期项目总建筑面积94.8万平方米一汽-大众汽车有限公司青岛工厂一期项目年产乘用车30万辆山东神州巨电新能源实业有限公司纯电动大巴动力锂电池产业化项目32年产纯电动大巴动力锂电池亿瓦时山东常林机械集团股份有限公司大型节能环保挖掘机产业化项目年产大型节能环保挖掘机5000台永佳动力股份有限公司环保节能型通用汽油机植保机械以及园林机械产品研发生产项目年产环保节能型通用汽油机、植保机械及园林机械600万台迈赫机器人自动化股份有限公司工业机器人及智能制造装备项目年产机器人系统及工作站台550套大国重器自动化设备山东股份有限公司机器人项目（年产机器1.05人万台）山东开泰工业科技有限公司海洋工程装备表面处理成套装备项目年产海洋工程装备表面处理成套装备1000台套威海普益船舶环保科技有限公司船舶废气洗涤脱硫设备生产项目年产镁基法船舶废气洗涤脱硫系统500套威海市海王旋流器有限公司节能环保技术装备制造项目年产旋流器等节能环保装备1.2万台套山东富力世新型材料有限公司智能自动轧制生产设备建设项目年产精密数控轧机63台、精密制管自动生产线300套山东双一科技股份有限公司模具产业化与车辆用复合材料制品生产项目（年产非金属模具35套风电机舱罩1000套、车辆用复合材料制品10万件）山东恒威电力设备有限公司非晶合金变压器及可控饱和电抗器项目年产非晶合金变压器500兆伏安、可控饱和电抗器1000台新兴重工临清天然气非管网科技生态产业园一期项目年产LNG撬装站400支、CNG液压子站100支东营圣亚生态能源科技有限公司生物燃气生态能源项目年产生物天然气6000万立方米山东哈迪斯汽车配件有限公司轨道列车空气弹簧减震总成项目年产轨道列车空气弹簧减震总成500万套青岛歌尔科技产业项目年产ASIC、MEMS芯片50亿只、可穿戴式计算机万2400套、智能机器人2200台烟台华安通信设备有限公司中韩信息产业园项目年产手机主板3600万件、手机2500万部山东创新金属科技股份有限公司铝合金电子材料项目年产高档铝合金电子材料1000万套山东新华制药股份有限公司现代医药国际合作中心项目年产固体制剂200亿片、粒、袋山东鲁抗医药股份有限公司高新生物技术产业园一期项目年产固体制剂53.8亿片、粉针13.2亿支山东新时代药业有限公司奥利司他产业化建设项目年产奥利司他片剂2亿片、胶囊剂4亿粒山东一方制药有限公司中药配方颗粒制造中心项目年产中药配方颗粒1800吨山东泰邦生物制品有限公司血液制品项目年产人凝血因子Ⅷ60万支、人凝血酶原复合物100万支、人纤维蛋白原72万支山东新华医疗器械股份有限公司医学影像产品产业化项目年产医学影像诊断设备380台套、治疗设备60台套威海威高血液净化制品有限公司高通量血液透析器产业化项目年产高通量血液透析器4000万支山东聊城阿华制药股份有限公司药用辅料一期项目年产药用辅料2.2万吨海斯摩尔生物科技有限公司医卫用生物质新材料及制品产业化项目年产壳聚糖纤维2000吨、医用非织造布2000吨、医用敷料1200万件烟台双塔食品股份有限公司高纯度蛋白项目年产高纯度蛋白6万吨谷神生物科技集团有限公司多肽蛋白项目年产多肽蛋白3万吨山东保康生物科技有限公司生姜蛋白酶等)种功能成分联合萃取项目年产生姜蛋白酶30吨、姜黄素9吨郯城安泰生物科技有限公司银杏叶提取物系列产品深加工项目年产抗氧化软胶囊5亿粒、银杏蜂胶山楂胶囊5亿粒、银杏叶饮料5000万瓶伟日山东生物科技有限公司乳酸链球菌素产业化项目年产乳酸链球菌素2000、吨乳酸钠1.8万吨山东新和成氨基酸有限公司蛋氨酸项目年产蛋氨酸10万吨赤山集团有限公司海洋生物制品精深加工与冷链物流基地建设项目年产海洋生物制品5万吨山东悦一生物科技有限公司鱼骨联产鱼骨素及衍生产品项目年产鱼骨素3000吨山东省滕州瑞达化工有限公司聚丁烯项目年产聚丁烯6万吨凯赛（金乡）生物材料有限公司绿色尼龙56项目年产绿色尼龙5620万吨山东农大肥业科技有限公司国家土壤修复计划示范基地项目年产黄腐酸钾5万吨、缓控释复合肥40万吨山田研磨材料有限公司功能性系列纳米粉体材料建设项目年产纳米粉体材料5000吨山东高速轨道设备材料有限公司GRTSⅢ型高铁轨道板项目年产GRTSⅢ型高铁轨道板7万块天鼎丰材料技术有限公司高强粗旦聚丙烯纺粘针刺土工布项目年产高强粗旦聚丙烯纺粘针刺土工布3.2万吨莱芜钢铁集团粉末冶金有限公司高性能合金特种粉末材料项目年产特种粉末冶金材料10万吨山东华盛荣镁业科技有限公司镁合金科技产业园项目年产镁合金系列产品6.3万吨临沂鑫海新型材料有限公司高镍基材料节能环保建设项目（年产高镍基节能环保材料120万吨）黄河三角洲现代农业孵化展示项目总建筑面积10.3万平方米泗水利丰甘薯全产业链产业融合示范项目总建筑面积6.9万平方米金利源现代农牧循环经济科技示范项目总建筑面积17.1万平方米齐鲁工业大学菏泽校区建设项目总建筑面积45.7万平方米烟台黄金职业学院项目总建筑面积22.7万平方米高密豪迈职业教育园区项目总建筑面积8.4万平方米日照市职业教育公共实训基地项目总建筑面积19.9万平方米曲阜干部学院项目总建筑面积8.1万平方米淄博市中心医院西院区建设项目(总建筑面积33.9万平方米)聊城鲁西南医院一期项目(总建筑面积11.1万平方米)文登整骨烟台医院建设项目(总建筑面积28.8万平方米)巨野县人民医院医养新院区建设项目(总建筑面积12.9万平方米)成武县养老康复中心项目(总建筑面积5.6万平方米)博山姚家峪生态养老中心项目(总建筑面积60.6万平方米)临沂鲁商国际健康城一期项目(总建筑面积15.3万平方米)中晨青州书画艺术城项目(总建筑面积53.6万平方米)济宁市文化中心一期建设项目(总建筑面积7.6万平方米)聊城市古城区博物馆文化建设项目(总建筑面积4.4万平方米)蓝树谷青少年社会职业体验中心一二期项目(总建筑面积3.6万平方米)无棣县全民健身活动中心项目(总建筑面积4.2万平方米)泰安市京沪高铁南片区改造和东平湖库区移民避险解困项目（总建筑面积211.1万平方米其中京沪高铁南片区D、E、F棚户区改造141.6万平方米,东平湖库区移民避险解困二期69.5万平方米)济南市海绵城市试点区域园林绿地系统建设和道路改造工程（改建道路23.2公里，景区保护、雨水收集等）乐陵市铁营镇改善农村人居环境建设项目（净水5万吨/日,污水处理2.5万吨/日,燃气管道42公里,道路78公里,改造农村住房、学校等20.4万平方米）滕州市高铁新区地下管廊建设项目（全长21公里）郓城县新型城镇化基础设施建设项目（新建道路59.8公里、桥梁11座，铺设排水管网,151公里，绿化面积,41.8万平方米）济南市英雄山路南段高架桥工程-顺河高架南延一期工程（全长2.3公里）。
保健食品中添加违禁药物情况及检测方法研究进展
保健食品中添加违禁药物情况及检测方法研究进展保健食品是近二十年在国内外兴起的新兴食品，系指具有特定保健功能的食品，即适用于特定人群食用，具有调节机体功能，不以治疗疾病为目的的食品。
近几年来，随着科学技术不断进步，保健食品生产工业技术水平不断提高，种类迅速增加，特别是我国加入WTO以后，国外企业纷纷抢占国内市场，进口保健食品品种和数量大幅度上升。
同时，该领域利用高技术手段做假的不法行为也时有发生。
据有关调查结果显示，近两年我国已知的非法添加药品、防腐剂及非食品成分的保健食品有200多种。
保健食品添加违禁成分或掺假，不仅导致不良后果引发的一系列问题和纠纷，而且在使用者不知情的条件下，将产生极大的毒副作用，不断引起人们对保健品背后隐患的担忧。
国家相关法律法规明令禁止在保健食品中添加药物；批准生产销售的保健食品，在其产品广告中禁止宣传疗效作用。
但现在市场上有些不法厂商，在保健食品中滥加药物，在广告中非法宣传疗效，欺骗和诱使消费者购买服用，致使当今滥用保健食品现象极为普遍。
殊不知，药品和保健食品是两个绝然不同的概念，误用加入药物的保健食品危害很大，这是应当引起人们清醒认识和严肃对待的问题。
本文介绍了可用和禁用于保健食品的中药、保健食品中常添加的违禁药物和危害，并就近年来保健食品中常添加的违禁药物检测方法的研究进展作一综述。
1 保健食品与一般食品和药品的区别[1]1.1 保健（功能）食品保健食品是指声称具有特定保健功能或者以补充维生素、矿物质为目的的食品，即适宜于特定人群食用，具有调节机体功能，不以治疗疾病为目的，并且对人体不产生任何急性、亚急性或者慢性危害的食品。
1.2保健（功能）食品和一般食品的区别保健食品与普通食品、药品有着本质的区别（表1），保健食品是指具有特定保健功能的食品。
作为食品的一个种类，保健食品具有一般食品的共性，既可以是普通食品的形态，也可以使用片剂、胶囊剂、颗粒剂、丸剂、口服液等多种特殊剂型，但保健食品的标签和说明书必须标示保健功能。
奥利司他(舒尔佳)-选择性抑制脂肪吸收可用于长期减肥(英文)
Received June 14, 2000; Accepted June 14, 2000.Author to whom all correspondence and reprint requests should be addressed:Dr. Jonathan Hauptman, Hoffmann-La Roche Inc., 340 Kingsland Street,Nutley, NJ 07110-1199. E-mail: jonathan.hauptman@201Orlistat is a novel, noncentrally acting antiobesity agent that selectively inhibits gastrointestinal lipase activity, thereby reducing the absorption of dietary fat by approximately one-third. In a series of 1- and 2-yr randomized, placebo-controlled trials of obese sub-jects, treatment with orlistat in combination with a mildly calorie-restricted diet consistently produced significantly greater mean weight loss than diet alone.More orlistat-treated subjects than placebo recipients achieved clinically meaning ful weig ht reduction (*5%or *10% of initial body weig ht) after 1 and 2 yr. Orlistat was also associated with a significant reduction in the regain of lost weight during long-term treatment. In addition, orlistat therapy resulted in sig nificant improvements in several cardiovascular risk factors including serum total and low-density lipoprotein–cholesterol, serum insulin levels, systolic and diastolic blood pressure, and waist circumference. Further-more, obese subjects with type 2 diabetes achieved a sig nificantly g reater decrease in body weig ht with orlistat compared with placebo, as well as significant improvements in HbA 1c and fasting g lucose levels.Among subjects with impaired g lucose tolerance,orlistat compared with placebo reduced the propor-tion who developed type 2 diabetes. Conversely,orlistat increased the proportion of subjects who achieved a normalization of g lucose tolerance. Orlistat acts locally in the g astrointestinal tract and is only minimally absorbed. In long -term clinical trials,orlistat was well tolerated by both diabetic and non-diabetic subjects.Key Words:Orlistat; antiobesity agents; fat-restricted diet; weight loss; coronary risk.IntroductionThe etiology of obesity is complex and involves the interplay of numerous environmental and genetic factors.However, obesity is essentially the consequence of a long-term positive energy balance in which energy intake exceeds energy expenditure.Dietary intake and composition, together with physical activity, are the primary modifiable factors that influence energy balance. In particular, the excessive consumption of dietary fat may have a major contributory role in the devel-opment of obesity (1–3). Dietary fat has a higher energy density than other macronutrients, providing 9 kcal/g (37kJ/g) compared with just 4 kcal/g (17 kJ/g) with either pro-tein or carbohydrate. Moreover, fat has only a weak effect on postprandial satiety. In studies of obese subjects, high-carbohydrate meals suppressed subsequent food intake to a greater extent than high-fat meals that were matched for energy density, volume, and sensory properties (4). In another study, obese patients who ate from a range of either high-fat or high-carbohydrate foods voluntarily consumed twice as much energy from the high-fat items (5). Several factors may play a role in the low satiating effect of fat,including stomach distension, nutrient absorption, hor-monal release, and oxidation of nutrients.Fat also tends to be very palatable, and studies have shown that both male and female obese individuals tend to report definite preferences for high-fat foods (6). This,together with the high energy density and low satiating effect of fat, can result in the overeating or passive overcon-sumption of high-fat foods.In addition, whereas the oxidation of both carbohydrate and protein is tightly correlated with intake, fat balance is less well controlled (7). Fat oxidation, unlike the oxidation of either carbohydrate or protein, is correlated with energy intake rather than fat intake (8,9). As a result, energy from fat leads to greater weight gain than calories from other macronutrients because they are less likely to be oxidized,and instead are readily stored as body fat. There is evidence to suggest that obese subjects have a reduced ability to oxidize fat in comparison with lean individuals. In one study, a 7-d high-carbohydrate diet resulted in a signifi-cant increase in carbohydrate oxidation in both obese and lean subjects. However, on a high-fat diet, fat oxidation increased among lean subjects but not obese subjects (10).In another study, previously obese women with a genetic predisposition toward obesity were less able to increase fat oxidation in response to increased dietary fat content com-pared with never-obese control subjects (11).OrlistatSelective Inhibition of Caloric Absorption Can Affect Long-Term Body Weight Jonathan HauptmanHoffmann-La Roche Inc., Nutley, NJOrlistat: Inhibition of Fat Absorption/Hauptman202EndocrineThe treatment of obesity involves the creation of a nega-tive energy balance in order to reduce body fat stores. Sev-eral studies have shown that low-fat diets can promoteweight loss in both lean and obese subjects, and ametaanalysis of 33 controlled studies of ad libitum low-fatdietary interventions reported that a 1% reduction in di-etary fat produced a 0.22-kg weight loss (3,12).H owever, long-term weight reduction is difficult tomaintain by dietary intervention alone, and most obesepatients eventually regain much of their lost weight (13,14).This may be partially attributed to compensatory physi-ologic processes that act to oppose weight loss and themaintenance of lower body weight. However, much of thefailure associated with conventional dietary and behavioralmodification is a direct result of the inability of many obeseindividuals to maintain long-term compliance with signifi-cant dietary and lifestyle changes.The limited success of dietary and behavioral interven-tions in long-term weight control has meant that adjunctivepharmacotherapy that is both well tolerated and effectivewill become increasingly important in the management ofobesity. One approach is the induction of weight loss bydrug-mediated inhibition of fat absorption. Orlistat(Xenical®, Hoffmann-La Roche Inc.), a novel, noncentrallyacting antiobesity agent, is a highly potent inhibitor of gas-trointestinal (GI) lipases, enzymes that play a crucial rolein the digestion of long-chain triglycerides. Orlistat pro-duces a partial inhibition of triglyceride hydrolysis and areduction in the subsequent absorption of free fatty acidsand monoglycerides (Fig.1) (15).The inhibitory effect of orlistat on dietary fat absorption has been evaluated using fecal fat excretion as a represen-tative pharmacodynamic parameter. The inhibition of dietary fat absorption with orlistat is dose dependent, with the optimal therapeutic dosage being 120 mg administered three times daily with main meals (16). This dosage consis-tently and reliably reduces the absorption of dietary fat by approximately one-third, resulting in a decrease in avail-able calories after ingestion (15).Orlistat is highly selective and has no significant inhibi-tory effect on the hydrolysis and absorption of carbohydrates, proteins, and phospholipids. In addition, the absorption of orlistat from the GI tract is minimal, and therefore orlistat has virtually no potential for an inhibitory effect on systemic lipase activity (17). Consequently, in contrast to some cen-trally acting appetite suppressants, adverse events owing to systemic drug absorption should be fewer with orlistat. Weight Loss and Prevention of Weight RegainIn clinical trials, treatment with orlistat in combination with a mildly calorie-restricted diet has consistently pro-duced significantly greater weight loss than diet alone in obese subjects. Unless otherwise stated, the results pre-sented subsequently come from the intent-to-treat popula-tion, which includes data from all patients who received at least one dose of study medication and had at least one follow-up efficacy assessment. In a multicenter, 2-yr, ran-domized, placebo-controlled trial conducted in the United States by Davidson et al. (18), 1187 obese men and women (body mass index (BMI) of 30–43 kg/m2) were enrolled in a 1-mo single-blind, placebo lead-in period during which they were encouraged to follow a mildly hypocaloric diet. This diet was designed to provide a 600 kcal/d energy defi-cit with 30% of calories as fat. Subjects (n= 892) who completed this dietary lead-in period were randomly assigned (in a 3:1 ratio) to treatment with 120 mg of orlistat (n= 668) or placebo (n= 224) three times daily for 1 yr. Subjects continued to follow the hypocaloric diet during the first year of double-blind treatment. After 1 yr, subjects treated with orlistat had achieved significantly greater mean weight loss than placebo recipients (8.8 vs 5.8% of initial body weight; p<0.001). Moreover, a significantly higher proportion of orlistat-treated subjects achieved a clinically meaningful weight loss of *5% (65.7 vs 43.6%; p<0.01) or *10% (38.9 vs 24.8%; p <0.05). In the second year of the study, orlistat subjects who completed the first year were rerandomized to three times daily treatment with orlistat (n= 153), half-dose orlistat (60 mg) (n= 152), or placebo (n= 138), while subjects who received placebo during yr 1 Fig. 1. Mode of action of orlistat. TG, triglyceride; MG, monoglyceride; FA, fatty acids.Orlistat: Inhibition of Fat Absorption/HauptmanVol. 13, No. 2203 continued to do so for a second year. In addition, all sub-jects were advised to follow a weight maintenance dietdesigned to promote stable body weight rather than con-tinue with their hypocaloric weight loss diet. Of subjectswho were treated with orlistat during the first year, thosewho were rerandomized to 120 mg of orlistat regained sig-nificantly less of their body weight during the second yearcompared with subjects rerandomized to placebo (35.2 vs63.4% weight regain; p<0.001). Treatment with 120 mg oforlistat for 2 yr resulted in mean weight loss of 7.6%, sig-nificantly greater than with 2 yr of placebo (4.5%; p<0.001). In addition, twice as many orlistat-treated sub-jects maintained a weight reduction of *10% after 2 yr(34.1 vs 17.5%; p <0.05).The weight loss efficacy of orlistat has also been demon-strated in European trials that shared a design and method-ology similar to that of the US study (19,20). In a 2-yr studyof 743 obese subjects (BMI of 28–47 kg/m2), significantly greater mean weight loss was achieved with orlistat plus diet compared to diet alone after 1 yr (10.2 vs 6.1%; p <0.001) (Fig.2) (19). More orlistat-treated subjects than placebo recipients achieved a weight loss of *5% (68.5 vs 49.2%), and twice as many subjects in the orlistat group as in the placebo group achieved a weight reduction of *10% (38.8 vs 17.7%). After 2 yr of treatment, subjects in the orlistat group achieved mean weight loss of 7.8%, com-pared with 4.6% in the placebo group. Twice as many orlistat-treated subjects as placebo recipients maintained a weight loss of *10% (33.8 vs 14.6%; p<0.05). In another 2-yr European study, a significantly greater weight reduc-tion was achieved with orlistat in conjunction with diet compared to diet alone after 1 yr (9.7 vs 6.6%; p<0.001). This significantly greater weight loss with orlistat was sus-tained after 2 yr (7.6 vs 4.5%; p <0.001) (20).As with the study by Davidson et al. (18), participants in both of these European studies switched from a weight loss diet to a weight maintenance diet for the second year. As expected, some regain of lost weight occurred during yr2. However, in both studies, weight regain was reduced by treatment with orlistat compared to placebo.In each of these three 2-yr randomized, controlled trials of orlistat, obese subjects were generally recruited at spe-cialist obesity clinics. However, in a further study, the ef-fect of orlistat was investigated among subjects in a primary care setting (21). A total of 796 obese subjects (BMI of 30–43 kg/m2) entered a 1-mo dietary lead-in period before being randomized to 120 mg of orlistat, 60 mg of orlistat, or placebo three times daily. Subjects were prescribed a hypocaloric diet during the first year of treatment and were switched to a weight maintenance diet for the second year. Unlike previous studies of orlistat, subjects were counseled by health care staff who had no specialist training in diet or obesity management.After 1 yr, subjects treated with 120 mg of orlistat had achieved significantly greater weight loss than placebo recipients (7.9 vs 4.2%; p<0.0001). Significantly greater weight loss with orlistat compared to placebo was sustained after 2 yr of treatment (5.0 vs 1.7%; p<0.0001). In addition, almost three times as many subjects in the orlistat group as in the placebo group maintained a weight loss of *10% after 2 yr (18.6 vs 6.6%; p<0.001). Mean weight reduction in this study, in both the orlistat and placebo groups, was slightly less than that achieved in other trials of orlistat (18,19). H owever, the additional weight loss effect of orlistat compared with diet alone in this study was similar, if not greater, than reported in other studies and suggests that orlistat may be an important adjunct in the manage-ment of obesity in primary care.The maintenance of lower body weight and the preven-tion of weight regain are essential components of success-ful long-term obesity management. In addition to the reduction in weight regain reported in 2-yr studies of orlistat, the effect of orlistat on weight regain has been specifically investigated in a large US multicenter study (22). Obese subjects (BMI of 28–43 kg/m2) were recruited at 17 clinical research centers and prescribed a hypocaloric diet (1000kcal/d deficit) designed to produce a weight loss of 0.5–1.0 kg/wk for a 6-mo period. On completion, sub-jects who had lost *8% of their body weight were random-ized to double-blind treatment with either placebo or 30, 60, or 120 mg of orlistat three times daily in combination with a weight maintenance diet for 1 yr. Of the 1313 sub-jects who entered the weight loss period, 729 achieved a weight reduction of *8% (mean weight loss of 10 kg) and entered the double-blind treatment period. After 1 yr, there was significantly less weight regain with 120 mg of orlistat compared to placebo (32.8 vs 58.7%; p <0.001).The effect of orlistat on body weight has also been dem-onstrated in a multicenter, US-based study of obese sub-jects with type 2 diabetes (23). Weight loss is an important goal of therapy for obese type 2 diabetes patients. However, diabetic patients often have greater difficulty than nondia-betic subjects in achieving clinically meaningful weight Fig. 2. Mean weight loss after 1 yr in obese patients randomized to double-blind treatment with 120 mg of orlistat (n= 343) or placebo (n= 340) plus a mildly hypocaloric diet. (Adapted from Sjöström et al. ref. 19.)Orlistat: Inhibition of Fat Absorption /Hauptman 204Endocrinereduction and maintaining lower body weight through di-etary restriction or behavioral modification (24–26).Weight loss may be especially difficult if patients are re-ceiving treatment with diabetic medications that promote weight gain, such as insulin or sulfonylureas (27,28).A total of 391 subjects with type 2 diabetes controlled with oral sulfonylureas entered a 5-wk lead-in period dur-ing which they received placebo and a nutritionally bal-anced mildly hypocaloric diet (500 kcal/d deficit) (23). On completion, subjects were randomized to either 120 mg of orlistat or placebo three times daily plus dietary interven-tion for 1 yr. Subjects treated with orlistat achieved signifi-cantly greater weight loss than placebo recipients (6.2 vs 4.3%;p <0.001). Furthermore, twice as many patients re-ceiving orlistat lost *5% of their initial body weight (49 vs 23%;p <0.001). Similarly, more orlistat-treated patients than placebo recipients achieved a weight reduction of *10% (17.9 vs 8.8%; p = 0.017).In addition to significantly greater weight loss, patients treated with orlistat also had a greater mean decrease in waist circumference in this study (–4.8 vs –2.0 cm; p <0.01).Waist circumference is a marker of visceral abdominal obesity (29). Excess visceral abdominal adipose tissue is associated with the insulin resistance syndrome, also known as the metabolic syndrome, and is an independent predictor of type 2 diabetes and coronary heart disease (30–32). Sig-nificant reductions in waist circumference after treatment with orlistat were also reported in studies of obese nondia-betic subjects (18,20).Effects of Orlistat on Cardiovascular Risk FactorsModerate weight loss of 5–10% is associated with improvements in several cardiovascular risk factors,includ-ing dyslipidemia, hypertension, hyperinsulinemia, glucose intolerance, and type 2 diabetes (33,34). The effects of weight management with adjunctive orlistat therapy on these coronary risk factors have been assessed in several clinical trials.DyslipidemiaIn the 2-yr study by Davidson et al. (18), patients treated with orlistat achieved significantly greater reductions in serum total and low-density lipoprotein (LDL)-cholesterol than placebo recipients. During the 4-wk dietary lead-in period, total and LDL-cholesterol declined by approx 8%.However, after randomization, total and LDL-cholesterol concentrations increased in the placebo group despite further weight loss, but continued to decline in the orlistat group.After 1 yr, reductions in total and LDL-cholesterol were sig-nificantly greater with orlistat vs placebo (p <0.001) (Fig.3).The improvements in total and LDL-cholesterol achieved with orlistat were independent of the greater weight loss with orlistat compared to placebo. This additional lipid-lowering effect of orlistat is probably related to the partial inhibition of fat absorption from the GI tract. A similar independent lipid-lowering effect was reported in the European trials of orlistat (19,20)as well as in the study of overweight subjects with type 2 diabetes (23).Blood PressureTreatment with orlistat is also associated with improve-ments in systolic and diastolic blood pressure (BP). Numerous studies have reported that clinically significant reductions in BP are achieved with moderate weight loss and that a weight reduction of just 5 kg can significantly reduce BP in obese patients with or without hypertension (35–37). In the David-son et al. (18)study, systolic BP was reduced to a signifi-cantly greater extent with orlistat than placebo after 1 yr (p = 0.002). Diastolic BP also decreased more in the orlistat group than in the placebo group (p = 0.009). Sjöström et al.(19), also reported significantly greater reductions in both systolic and diastolic BP after 1 yr of orlistat compared to placebo. The greater reductions in BP associated with orlistat treatment are consistent with the greater degree of weight loss experienced by the subjects.The effect of orlistat on BP has been further assessed ina metaanalysis of five phase III clinical trials of orlistatFig. 3. Mean (±SEM) changes in serum total and LDL-cholesterol in obese patients randomized to double-blind treatment with 120 mg of orlistat or placebo plus a mildly hypocaloric diet. (Reproduced with permission from ref. 18.)Orlistat: Inhibition of Fat Absorption /HauptmanVol. 13, No. 2205(38). Obese subjects were randomized to orlistat (n = 1559)or placebo (n = 1116) in combination with diet for 1 yr.Among patients who achieved 5% weight loss (59% of orlistat-treated subjects vs 41% of placebo-treated sub-jects), mean systolic and diastolic BPs were reduced by 7.1and 5.4mmHg, respectively, with orlistat (vs 6.7 and 4.5 mmHg, respectively, with placebo). By comparison,reductions in systolic and diastolic BP were substantially smaller in subjects losing <5% of their body weight.Insulin and Glucose MetabolismThere is considerable evidence to suggest that both hyper-insulinemia and hyperglycemia are independent risk factors for cardiovascular disease (39–41). Treatment with orlistat is associated with improvements in insulin and glucose metabolism. In studies of nondiabetic obese subjects, orlistat in combination with diet resulted in significantly greater improvements in levels of fasting serum insulin and glucose after 1 and 2 yr than treatment by dietary intervention alone (18,19). In addition, a metaanalysis of three randomized,placebo-controlled trials has shown that treatment with orlistat may have potential use in preventing or delaying the progression from impaired glucose tolerance to type 2 diabe-tes (42). A total of 650 obese subjects were randomized to double-blind treatment with orlistat or placebo in combina-tion with a mildly hypocaloric diet for 1 or 2 yr. Oral glucose tolerance tests were performed before and after treatment (average duration of follow-up of 587 d). Orlistat-treated subjects lost more weight than placebo-treated subjects (6.7vs 3.8 kg; p <0.001). Among subjects with impaired glucose tolerance at baseline, fewer progressed to diabetic status in the orlistat group than in the placebo group (3.0 vs 7.5%).Conversely, more subjects with impaired glucose tolerance at baseline achieved normal glucose tolerance after orlistat treatment (71.6%) compared with placebo (49.1%) (Fig.4).Treatment with orlistat was also associated with significantly greater reductions in the integrated glucose and insulin areas after oral glucose challenge.Type 2 DiabetesIn a 1-yr study of obese patients with type 2 diabetes by H ollander et al. (23), greater weight loss with orlistat compared to placebo was accompanied by a more marked improvement in glycemic control. H emoglobin A 1c decreased by 0.28% after randomization to orlistat treat-ment whereas the placebo group increased by 0.18%(p <0.001). Fasting glucose decreased by 0.02 mmol/L fol-lowing the use of orlistat whereas it increased by 0.54 mmol/L in the placebo group (p <0.001). In addition, patients treated with orlistat were able to reduce their average dose of sulfonylurea medication to a greater extent than placebo recipients (–23 vs –9%; p <0.05) and fewer orlistat-treated patients withdrew from the study as a result of poor glyce-mic control (2.5 vs 8.8% of patients).Treatment with orlistat also produced greater improve-ments in several serum lipid parameters than placebo in patients with type 2 diabetes. Total cholesterol, LDL-cho-lesterol, LDL:high-density lipoprotein–cholesterol ratio,apolipoprotein-B (all p <0.001), and triglycerides (p <0.05)were all reduced to a significantly greater degree in the orlistat group vs the placebo group after 1 yr.Safety of OrlistatBecause orlistat acts locally in the GI tract and is only minimally absorbed, it has not been shown to be associated with serious systemic adverse events such as those that have been reported with some centrally acting appetite suppressant drugs. Indeed, in clinical trials, orlistat has been shown to be well tolerated by both diabetic and nondia-betic obese subjects (18,19,23). Orlistat was, however,associated with a higher incidence of certain GI events that relate to its partial inhibition of fat absorption, such as fatty/oily stools and fecal urgency. These GI conse-quences of orlistat tended to be of mild to moderate inten-sity, transient, and limited to one to two episodes perpatient. Moreover, these effects mostly occurred withinFig. 4. Percentage of subjects with (A)improvement or (B)deterioration in oral glucose tolerance from randomization to end of treatment. The distribution of categorical status at the end point differed across treatments within the normal at baseline and impaired at baseline cohorts (p <0.05). IGT, impaired glucose tolerance. (Adapted from ref. 42.)Orlistat: Inhibition of Fat Absorption/Hauptman206Endocrinethe first 12 weeks of therapy, with half occurring within the first month. These findings, together with supportive anec-dotal evidence, suggest that the pharmacologic effect of orlistat on fat absorption may encourage long-term compli-ance with a reduced-fat diet (43).The inhibition of dietary fat absorption by one-third with orlistat could, theoretically, have a potential impact on lev-els of fat-soluble vitamins and `–carotene. However, in 2-yr clinical trials, mean levels of vitamins A, D, and E and `-carotene remained within clinical reference ranges (18,19). In the study by Davidson et al. (18), treatment with orlistat compared to placebo was associated with a slightly higher incidence of two or more consecutive low values of vita-mins A (2.5 vs 1.0% of subjects), D (5.8 vs 1.4%), and E (4.2 vs 0.5%) and `-carotene (4.5 vs 0.0%). Supplementa-tion with once-daily multivitamins restored vitamins to within normal ranges in those individuals who experienced low levels.ConclusionPartial inhibition of dietary fat absorption with orlistat has been shown to be a well-tolerated and effective option as an adjunct to mild dietary modification in the long-term management of obesity. In clinical trials, orlistat in con-junction with dietary intervention has consistently and reli-ably been associated with significantly greater weight loss than achieved with diet alone in obese subjects with and without type 2 diabetes. Moreover, significant improve-ments in several obesity-related coronary risk factors, including hypercholesterolemia, hypertension, glucose intolerance, and insulin resistance, have all been reported with orlistat treatment.References1.Lissner, L. and Heitmann, B. L. (1995). Eur. J. Clin. Nutr.49,79–90.2.Golay, A. and Bobbioni, E. (1997). Int. J. Obes.21(Suppl.),S2–S11.3.Bray, G. A. and Popkin, B. M. (1998). 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过劳肥 病情说明指导书
过劳肥病情说明指导书一、过劳肥概述过劳肥主要是因过度劳累、工作压力较大、饮食不规律、长期熬夜等因素导致的肥胖。
常见于记者、教师、律师、程序员等繁忙工作的职员。
常有体重增加、身材臃肿、怕热、多汗、气急等症状。
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其它名称：无相关中医疾病：暂无资料。
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是否纳入医保：部分药物、耗材、诊治项目在医保报销范围，具体报销比例请咨询当地医院医保中心。
遗传性：无发病部位：暂无资料。
常见症状：体重增加、身材臃肿、怕热、多汗、气急主要病因：过度劳累、工作压力较大、饮食不规律、长期熬夜等检查项目：体重指数（BMI）、腰臀比（WHR）、皮下脂肪堆积程度、血脂测定、皮质醇激素测定、B 超、X 线重要提醒：过劳肥可能会诱发内分泌疾病、心脑血管疾病，需及时治疗。
临床分类：暂无资料。
二、过劳肥的发病特点病因总述：主要与过度劳累、工作压力大、运动量少、睡眠不足、饮食不规律等因素有关。
基本病因：1、过度劳累长期的工作导致机体过度疲劳，饥饿感增加，从而引起食量上升。
2、工作压力大压力过大可能会导致内分泌紊乱，引起新陈代谢变慢，长期以往导致肥胖。
3、运动量减少大多数职场白领长时间坐位工作，缺乏运动，导致机体能量消耗减少，引起脂肪堆积。
4、睡眠不足长期加班熬夜，睡眠不足，可能会引发机体瘦素（肥胖荷尔蒙）分泌减少，导致变胖。
瘦素又名肥胖荷尔蒙，亦称瘦蛋白、抗肥胖因子、苗条素，主要由脂肪细胞分泌的一种激素样蛋白质，具有控制摄食、增加能量代谢等作用。
5、饮食不规律由于工作繁忙，不能定时吃饭，仅进食高热量零食。
此外，长期吃夜宵，也是引发过劳肥的原因之一。
危险因素：暂无资料。
诱发因素：暂无资料。
四、过劳肥的症状症状总述：主要与过度劳累、工作压力大、运动量少、睡眠不足、饮食不规律等因素有关。
典型症状：1、呼吸系统会出现气急、呼吸困难等。
2、骨骼由于脊柱负荷过重，可有增生性脊椎骨关节炎存在，使患者出现腰腿痛。
2021缓解2型糖尿病中国专家共识重点内容
2021缓解2型糖尿病中国专家共识重点内容2 型糖尿病（T2DM）一直被认为是一种遗传因素与环境因素相互作用所致、以高血糖为特征的进展性疾病，需要长期使用降糖药物治疗。
但近年来随着T2DM 疾病谱的改变和循证医学证据的不断积累，这一认识正在逐渐改变。
为帮助我国临床医生在超重或肥胖T2DM患者中，规范开展缓解T2DM 的临床治疗工作，促进相关研究的发展，使患者获得安全、有效的干预措施，特制定“缓解2型糖尿病中国专家共识”。
T2DM 缓解的定义推荐：T2DM缓解的定义采用2021年ADA“2型糖尿病缓解的定义和解释”中对T2DM缓解的定义。
（证据级别4，推荐级别D）2021年ADA发布“2 型糖尿病缓解的定义和解释”，建议将患者停用降糖药物至少3月后，HbA1c＜6.5% 作为T2DM 缓解的标准。
但在有些情况下，如存在血红蛋白变异、疾病影响红细胞生存时间以及HbA1c检测方法不规范等，HbA1c不能反映真实血糖水平，可以用FBG＜7.0mmol/L 或通过连续葡萄糖监测（CGM）估算的糖化血红蛋白（eA1c）＜6.5%，作为T2DM缓解的替代标准。
在确定处于T2DM缓解后，仍需要每年复查HbA1c。
T2DM 缓解的机制推荐：T2DM缓解与纠正肥胖或显著改善体重、脂肪肝、脂肪胰、IR、高胰岛素血症相关，并与纠正高糖毒性及胰岛β细胞去分化与转分化相关。
（证据级别2a，推荐级别：B）推荐：积极进行体重控制，使BMI达到正常水平。
T2DM伴肥胖患者建议减轻体重≥10kg（最好＞15kg）或减重≥10%。
（证据级别2a，推荐级别：B）T2DM 缓解的基本条件推荐：采用“ABCD”法评估T2DM缓解基本条件。
（证据级别4，推荐级别：D）解释➤排除特殊类型的糖尿病，包括皮质醇增多症、生长激素瘤、胰高血糖素瘤以及一些遗传因素导致的特殊类型糖尿病，这些类型糖尿病需针对其致病因素进行治疗，方可使糖尿病得到缓解。
➤排除自身免疫型糖尿病，这类糖尿病患者的胰岛β细胞功能，因受到持续的自身免疫攻击而进行性下降，患者的超重和肥胖比例较低。
药食同源中药治疗肥胖症的有效成分和机制研究进展
在 2003 年发布的《中国成人超重和肥胖症预防控
肪积聚过多和（或）分布异常、体重增加。2016 年的
菔子、荷叶）等，其作用机制主要分为 3 类：增加肠道蠕动，促使胆固醇排泄，从而减少脂肪摄入；激活 AMPK 信号通
路，引导体内脂肪正常分布；加速体内脂肪代谢，促使胆固醇、三酰甘油及低密度脂蛋白含量下降。本文可为药食
同源中药在防治肥胖症的临床应用及产品开发中提供参考。
关键词 肥胖；药食同源；中药；有效成分；作用机制
低 体 重 的 同 时 ，也 可 能 会 导 致 不 同 程 度 的 肝 肾 损
坐伤肉”之说，在《素问》奇病论
年老体弱
[4]203
Байду номын сангаас
久病正虚
先天禀赋
肺脾肾气虚
胃热脾虚
脾肾阳虚
胃热滞脾
缺乏运动
先天禀赋
脾气虚弱
脾虚不运
痰浊内聚，膏脂堆积
肥胖症
图 1 中医中肥胖症的发病机制
Figure 1 Pathogenesis of obesity in traditional Chinese medicine
1 中医对于肥胖症的认识
油，达到减肥的作用[7]。Lorcaserin 可通过选择性地刺
肥胖症始记载于《黄帝内经》，在《素问》的异法方
宜论篇[4]55 中写到“其民不衣而褐荐，华食而脂肥，故邪
不能伤其形体，其病生于内。”中医认为肥胖症存在多
种病机病因（见图 1）。
海正药业(杭州)有限公司二期生物工程项目
海正药业(杭州)有限公司二期生物工程项目环境影响报告书( 简写本)浙江环科环境咨询有限公司（原浙江环境保护科学设计研究院）国环评证：甲字第2003号二O一二年一月一、项目概况1、项目来源浙江海正药业股份有限公司创建于1956年，公司经50多年的发展，形成了高科技、国际化、富有社会责任的三大发展特色。
2008年7月被国家评为首批“创新型企业”、10月评为首批“国家高新技术企业”。
海正药业生产的原料药已出口30多个国家和地区，主导产品如柔红霉素、阿霉素、表阿霉素、丝裂霉素等抗肿瘤药已占领美国非专利药原料药市场60%以上的份额；抗寄生虫药阿佛菌素占领国际兽药市场40%以上的份额；降血脂药他汀类的生产规模和技术水平列居世界第二，达到世界同类产品67%以上的市场占有率。
公司是国内唯一一家由WHO指定的全球抗多重耐药性结核病药物生产企业，被礼来、E-默克、先正达、APP等多家国际一流公司设为全球化战略联盟。
至今，海正药业已有12种剂型、92种制剂产品、36种原料药获得了国家GMP证书，累计有18个品种通过美国FDA认证、14个品种通过欧盟COS认证、1个品种通过澳大利亚TGA认证、2个产品在俄罗斯和韩国注册，还有30多个品种正在申报之中。
海正药业(杭州)有限公司的前身是杭州海正药用植物有限公司，是海正药业富阳基地的投资平台之一。
海正药业富阳基地始建于2002年，目前区域开发面积约为650亩，主要包括制剂生产线(抗肿瘤、培南及抗结核)、100亿片剂生产线、发酵生产线(抗寄生虫药物生产线)及公用工程等。
目前海正药业富阳基地抗寄生虫药物生产线中的奥利司他、制剂线的年产100亿片片剂已经投入生产，抗寄生虫项目的其他产品也投入了试生产，其他项目仍处于施工建设中，具体包括杭州海正药用植物有限公司制剂高技术项目、基因项目。
随着中国医药市场放大，短期内生物制药的原材料具有较高的稀缺性，将出现供不应求的现象。
海正药业未来重点发展“发酵、酶工程、酶转化”工艺深度开发，塑造制造和成本竞争力。
一种新型减肥药物--奥利司他
一种新型减肥药物--奥利司他
杨义生;陈家伦
【期刊名称】《国际内分泌代谢杂志》
【年(卷),期】2000(020)006
【摘要】奥利司他(orlistat,商品名赛尼可),为胃肠道胰脂肪酶抑制剂,通过抑制胃肠道胰脂肪酶活性,减少饮食中约30%脂肪的吸收,而达到减轻体重的目的.奥利司他还能降低血压,调节血脂,改善血糖.已有资料表明,奥利司他是一种通过全新的作用机制,具有良好耐受性,疗效确切的新型减肥药物.
【总页数】3页(P318-320)
【作者】杨义生;陈家伦
【作者单位】上海第二医科大学附属瑞金医院,上海市内分泌研究所,上海,200025;上海第二医科大学附属瑞金医院,上海市内分泌研究所,上海,200025
【正文语种】中文
【中图分类】R589.205
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奥利司他项目简介
目录：合成、性质、临床疗效、不良反应、现状、应用前景、纯化工艺
1 合成
临床上使用的奥利司他原料药大多由天然的胰脂肪酶抑制剂(Lipstatin)还原来制备。
以化学全合成的方式将会进一步降低消费者的使用成本。
奥利司他的合成主要涉及3个关键中间体: (3S,4S)-3-己基-4-[(2R)-2-羟基十三烷基]氧杂环丁酮、(3S,4S)-3-己基-4-[(2R)-2-羟基-5-十三碳烯烷基]氧杂环丁酮和(3S,4S)-3-己基-4-[(2S)-2-羟基十三烷基]氧杂环丁酮。
2 性质
奥利司他化学名为（S）-2-甲酰胺-4-甲基-戊酸-（S）-1-{(2S，3S)-3-己基-4-氧代-氧杂环丁基]甲基}十二烷基酯，分子式为C29H53NO，CAS编号是96829-58-2。
奥利司他为白色结晶性粉末,几乎不溶于水,易溶于氯仿,极易溶于甲醇和乙醇,易于热解,熔点为40℃～42℃。
其分子是含有四个手性中心的非对映异构体,在波长处529nm,其乙醇溶液具负旋光性。
3 临床疗效
3.1奥利司他的减肥疗效
奥利司他是一种强效、专一、长效的胃肠道脂肪酶抑制剂。
在药理学研究中，奥利司他作为一种戊酮酸酶,能在胃和小肠腔内起作用，与胃和胰腺中脂酶活性位点的丝氨酸残基共价键合，有力抑制胰腺、胃肠中的羧基酯酶及磷脂酶Ａ2的活性,减慢胃肠道中食物脂肪水解为氨基酸及单酰基甘油的过程，从而阻断饮食中三分之一脂肪的水解和吸收，降低体内脂肪贮存而减轻体重。
3.2奥利司他对心血管危险因素的改善
奥利司他可显著降低甘油三酯、载脂蛋白B和LDL/HDL胆固醇之比;减少胰岛素抵抗、降低血糖等肥胖相关危险因素的影响。
奥利司他对数项血脂指标的影响与体重减轻的幅度无直接关系，这种特有的降低血脂的药理效应可能与减少了饮食中脂肪的吸收有关;对血糖改善的可能机理为减少了腹腔内脂肪、改善了血脂代谢状况、增加了胰岛素的敏感性、提高了胰岛素的效能。
奥利司他可显著降低空腹胰岛素水平。
4 不良反应
奥利司他总体耐受性良好,除一些胃肠道的不良反应外,耐受性与安慰剂相似。
奥利司他较常见的不良反应是胃肠道症状。
该反应的发生与药物阻止摄入脂肪吸收的药理作用有关,大多数症状较轻,多在治疗早期(前3个月)出现,为一般性患者可以耐受,不需停药。
5 现状
目前，奥利司他是全球唯一的OTC减肥药，全球超过40,000,000人服用并成功减重，是目前最畅销的减肥产品。
它是有效减肥，奥利司他可直接阻断人体对食物中脂肪的吸收，摄入的热能和脂肪一旦小于消耗，体内脂肪自然减少，从而达到减重的目的。
它是安全减肥，有效成分不进入血液循环，不作用于中枢神经，副作用较少，不会出现头晕、心慌、失眠、口干等情况。
6 应用前景
奥利其他肝损害概率低，并且效果明显，又十分安全。
奥利司他片于2011年3月正式在国内上市，称作伊宁曼，是国内唯一通过临床验证过的同类药物。
现在国内市场销售奥利司他胶囊的价格大约是200元/盒（120mg×21），市场前景非常广阔。
利用发酵、化学合成技术得到奥利司他产品，利润空间是很大的。
7 纯化工艺
7.1 结构
奥利司他的摩尔质量为495.73 g·mol⁻¹。
结构式如下。
7.2 处理工艺
奥利司他的粗品分析如下：
经检测后，发现粗品中奥利司他的纯度为87.37%。
经过前期对粗品的处理后，我们采用的是日本大曹公司的SP系列填料进行高压制备。
收集液中有可以达到99.69%纯度的样品，单杂为0.15%，其他杂质为0.16%，回收率为86.5%。
这为下一步的精制起到了很好的除杂作用。
下图为其中一个馏分的液相分析图谱。
7.3 总结
奥利司他粗品中杂质较多，对后期的精制工艺容易造成影响。
通过一步高压制备纯化，得到纯度可达到99.69%的奥利司他样品，达到生产要求。