University of Macau / Institute of Chinese Medical Sciences

Background: Ulcerative colitis (UC) occurs in remissions and relapses and requires frequent outpatient follow-ups for management by specialists. These visits may not always coincide with the need for attention leading to unnecessary outpatient visits, nonattendances, inadequate monitoring, patient dissatisfaction and increased costs. Self management and shared decision making with health professionals may help overcome such challenges. Use of printed patient education interventions as a self management technique in UC has been discussed in this review. Objectives: To determine the impacts and implications of printed patient education interventions on patient empowerment, improved patient care, decreased healthcare use without burden on primary care and its impact on saving costs. The applicability of such an intervention in context of Hong Kong will also be discussed. Methods: PubMed and ProQuest Health and Medicine Databases, and Google scholar search engine were searched for original studies reporting results of randomized controlled trials (RCTs) of use of printed patient education interventions in management of inflammatory bowel disease and ulcerative colitis. There was no limit put on publication dates. Results: Four RCTs were finalized for review. The studies named primary and secondary outcomes, some of which were common to more than one study, and included process evaluations. Knowledge of UC was evaluated as an outcome in two studies, quality of life in four, health related anxiety and depression in two, patient satisfaction in two, medication adherence in one, relapses experienced in one and healthcare use in three. Knowledge and patient satisfaction was found to significantly improve in two studies. Statistically significant reduction was found in healthcare use in 2 RCTs with one also reporting fewer visits to outpatient department and primary care. Results were statistically insignificant for quality of life, medication adherence, relapse length, reporting of relapses and health related anxiety and depression in different studies though further study of their long-term effects is warranted to be better demonstrate their potential benefits. Conclusion: The presently proposed printed materials used in the studies appear to produce modest benefits in self management of UC. As the idea of self management evolves with time, we would need to define the optimal format of printed intervention and ways for continuous reinforcement in patients, as, currently, UC management is a lifelong process. / published_or_final_version / Public Health / Master / Master of Public Health

No description available.

Thesis (MSocSc)--University of South Australia, 1997

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

目的：通過收集潰傷性結腸炎（ Ulcerative colitis, UC ）的相關研究文獻，認識本病的發病機制、病名源流、流行病學及相關中醫藥治療情況，了解2006-2016 年間UC 的中藥口服治療現狀和用藥規律，對本病的常用藥和證治規律做統計分析，為臨床治療和研究該病提供有價值的參考依據。方法：檢索〈中國期刊全文數據庫〉’搜集2006-2016 年間有關中醫藥治療潰傷性結腸炎的研究文獻，按照合理的納入和排除標準’選出符合要求的文章，用Microsoft Office Excel2013 軟件建立UC 中藥口服用藥規律數據庫，對文章中涉及的中藥進行用藥頻率、藥物性味歸經及藥物類型的統計分析，以認識UC 常用內服中藥的情況，分析其用藥和證治規律。結果： (1 ）按照文獻的納入和排除標準進行篩選，總共選出符合要求的文章137 篇，涉及口服治療潰、屬性結腸炎的中藥141 種，總藥物使用次數1623 次，常用藥物依次為：白術、甘草、黃連、白苟、木香、夜苓、黨參、白頭翁、當歸、黃良、憲政仁、陳皮、黃琴、敗醬草、地輸、黃柏、枳殼等。藥物分類以清熱藥和補虛藥為主，清熱藥中使用頻率最高的是清熱燥濕藥與清熱解毒藥，補虛藥中使用頻率最高的是補氣藥，藥性寒、溫頻率相仿，藥味以甘苦辛為主，用藥歸經多為肝經、脾經、胃經和肺經。結論： (1 ）常用口服治佇潰傷性結腸炎的藥物以清濕熱藥和補氣藥為主，排名前十的依次為：白術、甘草、黃連、白苟、木香、夜苓、黨參、白頭翁、當歸、黃皮。（ 2 ）潰傷性結腸炎證型特點：虛實互存、寒熱錯雜，本虛標實，脾虛為本、濕熱為標，實證者以濕熱窒滯、濁毒絡腸為主，而虛證多見氣血虧虛、脾胃虛弱。(3 ）治療應辨清寒熱、虛實、標本，實者清熱燥濕、解毒通絡，虛者調補氣血，健脾理究，並酌情配伍止血收澀等藥。關鍵詢：潰傷性結腸炎﹔中藥﹔規律﹔性味歸經

published_or_final_version / Pharmacology / Doctoral / Doctor of Philosophy

潰瘍性結腸炎 (UC) 是一種原因不明的炎症性腸道疾病，治療原則是減輕炎症，但UC的病因有多種，一般消炎藥物如柳氮磺胺吡啶 (sulfasalazine) 等治療都是單靶向並有嚴重副作用，故副作用低、多靶向藥物是必要的。 / Cathelicidin 是一種抗菌抗炎的肽。事實上，鼠的 cathelicidin (mCRAMP) 直腸給藥能緩解小鼠 UC。為了提高療效及方便給藥，mCRAMP 編碼被導入乳酸乳球菌中。乳酸乳球菌是一種能抵抗胃酸的乳酸益生菌，因此口服亦能生產及傳送 cathelcidin 到大腸。 / 小鼠用含3% 葡聚醣硫酸鈉 (DSS) 的水7天以誘導UC。小鼠隨機分為十組，各接受每日一次的口服製劑：(1) 水，(2) DSS，(3, 4) DSS + 10¹° cfu 有或沒有 nisin 誘導的乳酸乳球菌，(5-8) DSS + 10⁸ 或 10¹° cfu有 (N4I) 或沒有 nisin 誘導的 mCRAMP 編碼乳酸乳球菌，(9) DSS + 0.5% 羧甲基纖維素鈉 (CMC-Na) 及 (10) DSS + 600 mg/kg懸浮於0.5% CMC-Na 的 sulfasalazine。 / 研究對 UC 預防效果時，小鼠同時接受 DSS 及治療。所有益生菌製劑中，只有 N4I 能降低中性粒細胞浸潤、脂質過氧化和炎症細胞因子表達，同時保護腸隱窩及黏膜分泌層結構，減少細胞凋亡及腸道菌群。相比之下，sulfasalazine 能抑制炎症但不能阻止結腸結構損傷。 / 進一步研究治療效果時，小鼠在炎症形成後接受四天治療。N4I 能促進結腸黏膜恢復，改善結腸和黏液分泌層的結構。這些作用可能通過刺激細胞增殖和抑制凋亡造成。相對地，sulfasalazine 對結腸組織重組沒有影響。 / 為了研究 mCRAMP 直接消炎作用，小鼠巨噬細胞 RAW 264.7 被脂磷壁酸和脂多醣刺激以模仿 UC 時細菌引起的炎症。mCRAMP 能減輕腫瘤壞死因子-α分泌及IκBα磷酸化並抑制核因子-κB (NF-κB) 活化，炎症酶如誘導型一氧化氮合酶和環氧合酶-2的表達也減少了。mCRAMP可能直接抑制細菌毒素與受體結合和/或直接抑制 NF-κB 產生消炎作用。 / 在研究 mCRAMP 修復黏膜的作用中，證實 mCRAMP 通過 G 蛋白偶聯受體依賴途徑和間接激活表皮生長因子受體、激活下游絲裂原活化蛋白激酶而促進細胞遷移、加速癒合。 / 總括而言，本研究首次顯示mCRAMP編碼乳酸乳球菌對 UC 有保護和治療作用，其抗炎、抗菌及促進黏膜修復作用來自乳酸乳球菌分泌的mCRAMP。多靶向的mCRAMP編碼乳酸乳球菌具有很大潛力，是一種比標準藥物 sulfasalazine 更好的治療結腸炎製劑。 / Ulcerative colitis (UC) is an idiopathic inflammatory bowel disease (IBD). The mainstay of drug treatment is to relieve inflammation. However the aetiology of UC is multi-factorial while most of the anti-inflammatory drugs, such as sulfasalazine, aim at single target with severe side effects. Therefore, a multi-targeted drug with low systemic toxicity is warranted. / Cathelicidin, a host defense peptide, shows anti-microbial and anti-inflammatory effects. Indeed intra-rectal administration of mouse cathelicidin (mCRAMP) alleviated murine colitis. To improve therapeutic efficacy and reduce inconvenience of administration, Lactococcus lactis (L. lactis) was constructed to encode cathelicidin. L. lactis is a lactic acid probiotic which could resist gastric acid and be able to produce and deliver cathelicidin to the colon when given orally. / Murine colitis was induced by 3% dextran sulphate sodium (DSS) given in drinking water for 7 days. Mice were given intragastrically with the following preparations once daily: (1) water, (2) DSS, (3, 4) DSS + 10¹° cfu L. lactis with or without nisin induction, (5-8) DSS + 10⁸ or 10¹° cfu mCRAMP-encoding L. lactis with (N4I) or without nisin induction, (9) DSS + 0.5% sodium carboxymethylcellulose (CMC-Na) and (10) DSS + 600 mg/kg sulfasalazine suspended in 0.5 % CMC-Na. / To study the preventive effects, mice received the above treatments together with DSS administration. N4I but not the other probiotic preparations suppressed inflammation by reducing neutrophil infiltration, lipid peroxidation and inflammatory cytokines expressions. Crypt structure and mucus-secreting layer were conserved together with the reduction of apoptosis and intestinal microbiota. In contrast, sulfasalazine could only suppress inflammation but not the destruction of colonic structure. / To further examine the therapeutic effects, mice received treatments for 4 consecutive days after the inflammation formation. Similarly, only N4I promoted colonic mucosal recovery and preserved colon structure and mucus-secreting layer. These actions are likely mediated through cell proliferation stimulation and apoptosis suppression. Again, sulfasalazine had no effects on colon tissue reconstitution. / The direct anti-inflammatory action of mCRAMP was also studied. Mouse macrophage RAW 264.7 cells were stimulated by lipoteichoic acid and lipopolysaccharide to mimic bacteria-induced inflammation during UC. mCRAMP prevented tumour necrosis factor-α secretion and IκBα phosphorylation followed by nuclear factor-κB (NF-κB) suppression. The inflammatory enzymes including inducible nitric oxide synthase and cyclooxygenase-2 were also reduced. It was postulated that mCRAMP might directly interact with the bacterial toxins to reduce receptor complex binding and/or reduce NF-κB suppression in macrophages. / The repairing action of mCRAMP on mucosal damage was studied in mouse colon cells. mCRAMP incubation reduced the wound size by promoting cell migration through the G-protein coupled receptor and epidermal growth factor receptor transactivation followed by the mitogen-activated protein kinases activation. / In conclusion, the present study demonstrates for the first time the protective and therapeutic roles of mCRAMP-encoding L. lactis in UC. It was the mCRAMP secreted from the probiotic to produce both anti-inflammatory and anti-bacterial actions and further promote mucosal repair. mCRAMP-encoding L. lactis is a multi-targeted agent for IBD. It has a great potential to be a new therapeutic agent better than sulfasalazine for the treatment of UC. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Wong, Ching Man. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 227-250). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese. / Abstract --- p.i / Acknowledgement --- p.v / Table of Content --- p.vi / List of Abbreviations --- p.xiii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Ulcerative Colitis --- p.1 / Chapter 1.1.1 --- Overview --- p.1 / Chapter 1.1.2 --- Epidemiology --- p.2 / Chapter 1.1.3 --- Diagnosis --- p.2 / Chapter 1.1.3.1 --- Clinical Presentation --- p.2 / Chapter 1.1.3.2 --- Apparative Diagnostics --- p.3 / Chapter 1.1.3.3 --- Innovative Diagnostics in IBD --- p.4 / Chapter 1.1.4 --- Etiopathogenesis --- p.4 / Chapter 1.1.4.1 --- Genetic Predisposition --- p.4 / Chapter 1.1.4.2 --- Environmental Factors --- p.5 / Chapter 1.1.4.2.1 --- Life Style --- p.5 / Chapter 1.1.4.2.1.1 --- Smoking --- p.5 / Chapter 1.1.4.2.1.2 --- Diet --- p.6 / Chapter 1.1.4.2.1.3 --- Hygiene --- p.6 / Chapter 1.1.4.2.1.4 --- Psychological Stress --- p.6 / Chapter 1.1.4.2.1.5 --- Appendectomy --- p.7 / Chapter 1.1.4.2.2 --- Colonic Mucus --- p.7 / Chapter 1.1.4.2.3 --- Non-steroidal Anti-inflammatory Drugs (NSAIDs) --- p.7 / Chapter 1.1.4.3 --- Alteration of Intestinal Microbiota --- p.8 / Chapter 1.1.4.4 --- Immune Factors --- p.10 / Chapter 1.1.5 --- Existing Treatments --- p.10 / Chapter 1.1.5.1 --- 5-Aminosalicyclic Acid --- p.11 / Chapter 1.1.5.2 --- Corticosteroids --- p.12 / Chapter 1.1.5.3 --- Immunomodulators --- p.12 / Chapter 1.1.5.4 --- Surgical Management --- p.13 / Chapter 1.1.6 --- Emerging Treatments --- p.14 / Chapter 1.1.6.1 --- Antibiotics --- p.14 / Chapter 1.1.6.2 --- Probiotics --- p.14 / Chapter 1.1.6.3 --- Nicotine Patches --- p.14 / Chapter 1.1.6.4 --- Butyrate --- p.14 / Chapter 1.1.6.5 --- Biological Therapies --- p.15 / Chapter 1.1.7 --- Risk of Colorectal Cancer --- p.17 / Chapter 1.2 --- Cathelicidin --- p.17 / Chapter 1.2.1 --- Cathelicidin Family --- p.17 / Chapter 1.2.2 --- Actions and Possible Mechanisms --- p.19 / Chapter 1.2.3 --- Cathelicidin in Ulcerative Colitis --- p.20 / Chapter 1.3 --- Probiotics --- p.21 / Chapter 1.3.1 --- Lactic Acid Bacteria --- p.21 / Chapter 1.3.2 --- Definition of Probiotics --- p.22 / Chapter 1.3.3 --- Possible Mechanisms of Action of Probiotics --- p.23 / Chapter 1.3.3.1 --- Mucous Layer --- p.23 / Chapter 1.3.3.2 --- Host Cell Antimicrobial Peptides --- p.25 / Chapter 1.3.3.3 --- Probiotic Antimicrobial Factors --- p.25 / Chapter 1.3.3.4 --- Epithelial Adherence --- p.27 / Chapter 1.3.4 --- Recent Findings in Ulcerative Colitis Treatment --- p.28 / Chapter 1.4 --- Lactococcus lactis --- p.29 / Chapter 1.4.1 --- Overview --- p.29 / Chapter 1.4.2 --- Gene Expression System --- p.30 / Chapter 1.4.3 --- Nisin-Inducible Controlled Gene Expression (NICE) System --- p.31 / Chapter 1.4.4 --- Recent Studies of Treating Ulcerative Colitis with L. lactis and Recombinant L. lactis --- p.32 / Chapter 1.4.5 --- Safety Concern of the Use of Probiotics and Transgenic Probiotics --- p.33 / Chapter 1.5 --- Aims --- p.35 / Chapter Chapter 2 --- Material and Methodology --- p.36 / Chapter 2.1 --- General Materials --- p.36 / Chapter 2.1.1 --- Chemicals --- p.36 / Chapter 2.1.2 --- Antibodies and Commercial Kits --- p.41 / Chapter 2.1.3 --- Bacteria --- p.43 / Chapter 2.1.4 --- Animals --- p.43 / Chapter 2.1.5 --- Cell Lines --- p.44 / Chapter 2.1.5.1 --- Mouse Colonic Epithelial Cells --- p.44 / Chapter 2.1.5.2 --- Mouse Macrophages --- p.44 / Chapter 2.2 --- Experimental Designs --- p.45 / Chapter 2.2.1 --- Construction of mCRAMP-Encoding Lactococcus lactis --- p.45 / Chapter 2.2.1.1 --- Enumeration of L. lactis --- p.45 / Chapter 2.2.1.2 --- Bacteriostatic Effect of mCRAMP on L. lactis --- p.46 / Chapter 2.2.1.3 --- Construction of mCRAMP-Encoding L. lactis --- p.46 / Chapter 2.2.1.4 --- Detection of mCRAMP Production by Western Immunoblotting --- p.50 / Chapter 2.2.2 --- In vivo Studies --- p.52 / Chapter 2.2.2.1 --- Survival of mCRAMP-Encoding L. lactis in Murine Colon --- p.52 / Chapter 2.2.2.2 --- Toxicity of mCRAMP-Encoding L. lactis --- p.53 / Chapter 2.2.2.3 --- Determination of mCRAMP Expression in Colon Tissue --- p.53 / Chapter 2.2.2.4 --- Induction of Colitis --- p.54 / Chapter 2.2.2.5 --- Probiotic and Sulfasalazine Treatment --- p.54 / Chapter 2.2.2.6 --- Clinical Symptoms --- p.56 / Chapter 2.2.2.7 --- Morphological Analysis --- p.56 / Chapter 2.2.2.7.1 --- Haematoxylin-Eosin (H&E) Staining --- p.56 / Chapter 2.2.2.7.2 --- Periodic Acid-Schiff (PAS) Staining --- p.58 / Chapter 2.2.2.8 --- Assessment of Apoptosis and Proliferation by Immunohistochemistry --- p.60 / Chapter 2.2.2.8.1 --- Determination of Cell Apoptosis by Terminal Deoxynucleotidyl Transferase dUTP Nick-end Labeling --- p.60 / Chapter 2.2.2.8.2 --- Determination of Cell Proliferation by Proliferating Cell Nuclear Antigen (PCNA) Staining --- p.61 / Chapter 2.2.2.9 --- Determination of the Degree of Inflammation --- p.63 / Chapter 2.2.2.9.1 --- Colonic Myeloperoxidase (MPO) Activity --- p.63 / Chapter 2.2.2.9.2 --- Colonic Malondialdehyde (MDA) Level --- p.63 / Chapter 2.2.2.10 --- Fecal Microbiota Count --- p.64 / Chapter 2.2.2.11 --- mRNA Expression of Inflammatory Cytokines --- p.64 / Chapter 2.2.3 --- In vitro Studies --- p.66 / Chapter 2.2.3.1 --- Determination of Anti-inflammatory Effects of mCRAMP --- p.66 / Chapter 2.2.3.1.1 --- Cell Viability --- p.66 / Chapter 2.2.3.1.2 --- Determination of TNF-α Secretion under Stimulation of LTA and LPS --- p.66 / Chapter 2.2.3.1.3 --- Effects of mCRAMP on TNF-α Secretion Under Stimulation of LTA or LPS --- p.67 / Chapter 2.2.3.1.4 --- Effects of Pertussis Toxin (PTX) on the Inhibition of TNF-α Secretion by mCRAMP --- p.67 / Chapter 2.2.3.1.5 --- Nuclear Factor-κB (NF-κB) Luciferase Reporter Gene Assay in RAW 264.7 cells --- p.68 / Chapter 2.2.3.1.6 --- Determination of IκBα Expression and Phosphorylation by Western Immunoblotting --- p.69 / Chapter 2.2.3.1.7 --- Determination of Inducible Nitric Oxide Synthases (iNOS) and Cyclooxygenase-2 (COX-2) Expression by Western Immunoblotting --- p.70 / Chapter 2.2.3.2 --- Determination of Wound Healing Effects of mCRAMP --- p.72 / Chapter 2.2.3.2.1 --- Cell Viability --- p.72 / Chapter 2.2.3.2.2 --- Cell Migration --- p.74 / Chapter 2.2.3.2.3 --- Determination of Epidermal Growth Factor Receptor (EGFR), Extracellular Signal-Regulated Protein Kinase (ERK1/2) and p38 Expression and Phosphorylation by Western Immunoblotting --- p.76 / Chapter 2.3 --- Statistical Analysis --- p.76 / Chapter Chapter 3 --- Result --- p.77 / Chapter 3.1 --- Protective Effects of Cathelicidin-Encoding Lactococcus lactis in Murine Ulcerative Colitis --- p.77 / Chapter 3.1.1 --- Introduction --- p.77 / Chapter 3.1.2 --- Results --- p.79 / Chapter 3.1.2.1 --- Survival of mCRAMP-Encoding L. latis in Murine Colon --- p.79 / Chapter 3.1.2.2 --- Detection of mCRAMP-Encoded by L. lactis in vivo --- p.81 / Chapter 3.1.2.3 --- Toxicity of mCRAMP-Encoding L. lactis --- p.84 / Chapter 3.1.2.4 --- Clinical Symptoms --- p.86 / Chapter 3.1.2.5 --- Histology Evaluation --- p.89 / Chapter 3.1.2.6 --- Apoptosis --- p.93 / Chapter 3.1.2.7 --- Determination of mCRAMP Expression in Colon Tissue --- p.96 / Chapter 3.1.2.8 --- Determination of the Degree of Inflammation --- p.101 / Chapter 3.1.2.9 --- Faecal Microbiota Populations --- p.105 / Chapter 3.1.3 --- Discussion --- p.108 / Chapter 3.2 --- Therapeutic Effects of Cathelicidin-Encoding Lactococcus lactis in Murine Ulcerative Colitis --- p.113 / Chapter 3.2.1 --- Introduction --- p.113 / Chapter 3.2.2 --- Results --- p.115 / Chapter 3.2.2.1 --- Clinical Symptoms --- p.115 / Chapter 3.2.2.2 --- Histology Evaluation --- p.117 / Chapter 3.2.2.3 --- Cell Death and Proliferation in Colitis --- p.123 / Chapter 3.2.2.4 --- Determination of mCRAMP Expression in Colon Tissues --- p.127 / Chapter 3.2.2.5 --- Determination of the Degree of Inflammation --- p.130 / Chapter 3.2.2.6 --- Faecal Microbiota Populations --- p.133 / Chapter 3.2.3 --- Discussion --- p.135 / Chapter 3.3 --- Mechanistic Study of the Anti-inflammatory Effects of mCRAMP in Mouse Macrophages --- p.139 / Chapter 3.3.1 --- Introduction --- p.139 / Chapter 3.3.2 --- Results --- p.145 / Chapter 3.3.2.1 --- Viability of Macrophages --- p.145 / Chapter 3.3.2.2 --- Effects of LTA and LPS on Tumour Necrosis Factor-α (TNF-α) Release from Macrophages --- p.150 / Chapter 3.3.2.3 --- The Inhibition of TNF-α Secretion by mCRAMP --- p.153 / Chapter 3.3.2.4 --- Inhibition of TNF-α Secretion by mCRAMP Independent to GPCR Stimulation --- p.158 / Chapter 3.3.2.5 --- Activation of NF-κB Through Detection of Luciferase Activity --- p.163 / Chapter 3.3.2.6 --- Determination of the Expression and Phosphorylation of IκBα by Western Immunoblotting --- p.166 / Chapter 3.3.2.7 --- Determination of iNOS and COX-2 Expression by Western Immunoblotting --- p.169 / Chapter 3.3.2.8 --- The Suppression of iNOS and COX-2 Expression by mCRAMP was Independent to GPCR and P2X₇ Signalling --- p.183 / Chapter 3.3.3 --- Discussion --- p.188 / Chapter 3.4 --- Mechanistic Study on Wound Healing Effect of mCRAMP in Mouse Colon Epithelial Cells --- p.193 / Chapter 3.4.1 --- Introduction --- p.193 / Chapter 3.4.2 --- Results --- p.196 / Chapter 3.4.2.1 --- Cell Viability --- p.196 / Chapter 3.4.2.1.1 --- MTT Assay --- p.196 / Chapter 3.4.2.1.2 --- BrdU Incorporation --- p.200 / Chapter 3.4.2.2 --- Cell Migration --- p.202 / Chapter 3.4.2.3 --- Determination of Epidermal Growth Factor Receptor (EGFR), Extracellular Signal-Regulated Protein Kinase (ERK1/2) and p38 Expression and Phosphorylation by Western Immunoblotting --- p.210 / Chapter 3.4.3 --- Discussion --- p.215 / Chapter 4 Discussion and Future Perspectives --- p.219 / Publications --- p.224 / References --- p.227

A dextran sulphate (DS) model of ulcerative colitis was used to examine the effects of macronutrient restriction with (MR+PRO) and without (MR) probiotic supplementation (VSL#3RTM) on protein metabolism and growth. MR and MR+PRO decreased weight and chest circumference gain, but had no effect on linear growth of piglets. MR decreased the protein fractional synthesis rate (FSR) of liver, masseter, longissimus dorsi, colon, as well as plasma albumin, measured by stable isotope tracer L-[ring-2H 5]phenylalanine. MR+PRO increased the FSR of hepatic proteins by greater than 70% and increased both the FSR and absolute synthesis rate (ASR) of the total plasma protein pool, albumin and fibrinogen. Over 11 days, MR+PRO piglets showed a smaller decrease in plasma total protein concentrations than WN piglets, and maintained higher albumin levels than either WN or MR piglets. These findings highlight the importance of adequate nutrition during gastrointestinal inflammation and show that when food intake is decreased, probiotics stimulate liver protein synthesis and increase the acute phase protein response, similar to the well-nourished state.

Thesis (M.S.P.H.)--University of Michigan, 1941.