published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

Daughters of gestational diabetes (GDM) affected pregnancies are at greater risk for the development of type 2 diabetes mellitus (DM) later in life. Adiponectin is an early marker of DM risk. Dietary fat quality has been proposed to be involved in the development of insulin resistance. Plasma fatty acids are a marker of recent dietary exposure. The objectives of this research were to determine whether differences in adiponectin exist in daughters of GDM pregnancies, and to describe how dietary fatty acids impact adiponectin concentrations. Fasting adiponectin and plasma fatty acids were examined for 180 adolescent daughters born to mothers with and without GDM. No differences were observed in adiponectin between study groups, however; a significant difference was detected upon comparison of daughters from mothers who were presently diabetic with those from healthy mothers. The association between fatty acids and adiponectin varied by visceral adiposity. Adiponectin was inversely associated with monounsaturated and omega-3 (n-3) fatty acids in the high waist group. Further knowledge on the interactions between fatty acids, desaturase activity and adiponectin would be helpful in planning early interventions for individuals at risk for diabetes.

Thesis (M.Med.Sc.)--University of Hong Kong, 2003. / Includes bibliographical references (leaves 46-57). Also available in print.

Made available in DSpace on 2016-08-12T18:48:41Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-02-26. Added 1 bitstream(s) on 2016-08-12T18:50:55Z : No. of bitstreams: 1 000865246.pdf: 1418887 bytes, checksum: e6ebb1960afe82f4c1dcbbf2458c4f2b (MD5) / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / Os compostos bioativos do arroz variam de acordo com a variedade e condições de cultivo. Componentes lipossolúvies como γ-orizanol, tocoferóis, tocotrienóis, carotenóides e ácidos graxos foram analisados em variedades de arroz integral, integral açucarado, vermelho e negro, utilizando métodos estabelecidos de cromatografia líquida de alta pressão e cromatografia gasosa. Todas as amostras também foram submetidas a análise por cromatografia líquida acoplada a espectrometria de massa (LTQ-Orbitrap XL), para identificar a abundância iônica [M-H]- de γ-orizanol, variando de m/z 573.3949 a 617.4211. O maior conteúdo de tocoferóis (α-, 1.5; γ-, 0.5 mg/100 g) e carotenóides (luteína 244; trans-β caroteno 25 μg/100 g) foram observados no arroz negro; tocotrienóis (α-, 0.07; γ-, 0.14 mg/100 g) em arroz vermelho e γ-orizanol (115 mg/100 g) no arroz integral açucarado. Em todas as amostras de arroz integral coloridas, os principais ácidos graxos encontrados foram palmítico (16:0), oleico (18:1n-9) e linoleico (18:2n-6). A análise dos componentes de γ-orizanol por espectrometria de massa permitiu identificar 3, 10, 8, e 8 álcoois triterpenóides ou esteril ferulatos nas amostras integral, integral açucarado, vermelho e negro, respectivamente. Estas identificações dos componentes de γ-orizanol, assim como, a concentração dos compostos bioativos, pode levar a elucidação das funções biológicas de cada componente à nível molecular. O consumo de amostras de arroz integral colorido, ricas em compostos bioativos benéficos, pode representar uma interessante estratégia dietética para melhoria da saúde / Bioactive components in rice vary depending on the variety and growing condition. Fat-soluble components such as γ-oryzanol, tocopherols, tocotrienols, carotenoids and fatty acids were analyzed in brown, sugary brown, red and black rice varieties using established high-performance liquid chromatography (HPLC) and GC methodologies. In addition, these colored rice varieties were further analyzed using a high-resolution liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS) (LTQ-Orbitrap XL) to identify the [M-H]- ions of γ-oryzanol, ranging from m/z 573.3949 to 617.4211. The highest content of tocopherols (α-, 1.5; γ-, 0.5 mg/100 g) and carotenoids (lutein 244; trans-β carotene 25 μg/100 g) were observed in black rice; tocotrienols (α-, 0.07; γ-, 0.14 mg/100 g) in red rice, and γ-oryzanol (115 mg/100 g) in sugary brown rice. In all colored rice varieties, the major fatty acids were palmitic (16:0), oleic (18:1n-9), and linoleic (18:2n-6) acids. When the γ-oryzanol components were further analyzed by LC-MS/MS, 3, 10, 8, and 8 triterpene alcohols or sterol ferulates were identified in brown, sugary brown, red, and black rice varieties, respectively. Such structural identification can lead to the elucidation of biological function of each component at the molecular level. Consumption of colored rice rich in beneficial bioactive compounds may be a useful dietary strategy for achieving optimal health / CNPq: 20013-8/140083-GM/GD

Dados recentes apontam para a participação do sistema renina-angiotensina (SRA) em processos metabólicos, devido a sua presença local em tecidos metabolicamente ativos, como o tecido adiposo, e sugerem que tais tecidos também poderiam ser alvos dos bloqueadores do SRA. Por isso, investigamos possíveis efeitos diretos de bloqueadores do SRA no metabolismo celular de adipócitos isolados. Para isso, adipócitos isolados foram tratados com doses não tóxicas de Alisquireno ou Captopril ou Losartan. Após 24 horas, as capacidades lipolíticas, lipogênicas e oxidativas foram. Como resultados, o fármaco Alisquireno, aumentou a relação entre oxidação de glicose e incorporação desse substrato em lipídeos, enquanto o Captopril diminuiu a incorporação de glicose em lipídeos, particularmente na fração glicerol do TAG mediante estímulo com insulina, bem como diminuiu a expressão gênica de receptor de (pró) renina. Como conclusão, os fármacos Captopril e Alisquireno podem modular o metabolismo lipogênico e oxidativo de adipócitos isolados, mas de maneiras diferentes. / Recent data indicate a participation of the renina-angiotensin system (RAS) in metabolic process, due its local presence in tissues, like the adipose tissue, and suggests that these tissues could be targets of RAS blockers. Therefore, we have studied the possible effects of pharmacological RAS blockers in isolated fat cells. Therefore, fat cells were isolated of epididymal fat pad and treated with non toxic doses of Aliskiren or Captopril or Losartan. After 24 hours, the lipolytic, lipogenic and oxidative capacity were tested in their respective spontaneous and stimulated states. Also, gene expression of PPARg and RAS components were verified. The results showed Aliskiren increases the relation between oxidation and lipogenesis from glucose, whereas Captopril decreased glucose lipid incorporation, especially in glicerol fraction of triglyceride when insulin stimulus exist, and the Renin receptor gene expression. As a conclusion, Captopril and Aliskiren can directly modulate lipogenic and oxidative metabolism of isolated fat cells, but in a different way.

No description available.

Li, Sui Mui. / On t.p. "beta" appears as the Greek letter. / Thesis submitted in: December 2006. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 182-189). / Abstracts in English and Chinese. / Abstract --- p.i / Abstract (Chinese) --- p.iii / Acknowledgements --- p.v / Table of contents --- p.vi / List of figures --- p.xii / List of appendices --- p.xix / Abbreviations --- p.xx / Chapter Chapter 1 --- General Introduction --- p.1 / Chapter Chapter 2 --- Role of PPARP in adipocyte differentiation - an in vitro study --- p.20 / Chapter 2.1 --- Introduction --- p.21 / Chapter 2.2 --- Materials and Methods --- p.23 / Chapter 2.2.1 --- Preparation ofPPARβ (+/+) and PPARβ (-/-) MEFs --- p.23 / Chapter 2.2.1.1 --- Materials --- p.23 / Chapter 2.2.1.2 --- Methods --- p.23 / Chapter 2.2.1.2.1 --- Isolation of MEFs --- p.23 / Chapter 2.2.1.2.2 --- Passage ofMEF culture --- p.25 / Chapter 2.2.2 --- Genotyping of PPARβ (+/+) and PPARβ (-/-) MEFs --- p.25 / Chapter 2.2.2.1 --- Materials --- p.26 / Chapter 2.2.2.2 --- Methods --- p.26 / Chapter 2.2.2.2.1 --- Primer design --- p.26 / Chapter 2.2.2.2.2 --- Genomic DNA extraction --- p.27 / Chapter 2.2.2.2.3 --- PCR reaction --- p.29 / Chapter 2.2.3 --- Western blotting of PPARβ(+/+) and PPARβ (-/-) MEFs --- p.30 / Chapter 2.2.3.1 --- Materials --- p.30 / Chapter 2.2.3.2 --- Methods --- p.31 / Chapter 2.2.3.2.1 --- Preparation of nuclear extracts --- p.31 / Chapter 2.2.3.2.2 --- Western blot --- p.32 / Chapter 2.2.4 --- Induction of adipocyte differentiation of PPARβ (+/+) and PPARβ(-/-) MEFs --- p.33 / Chapter 2.2.4.1 --- Materials --- p.34 / Chapter 2.2.4.2 --- Methods --- p.34 / Chapter 2.2.4.2.1 --- Seeding ofMEFs --- p.34 / Chapter 2.2.4.2.2 --- Adipocyte differentiation --- p.35 / Chapter 2.2.5 --- Oil Red O staining of differentiated PPARβ(+/+) and PPARβ(-/-) MEFs --- p.36 / Chapter 2.2.5.1 --- Materials --- p.36 / Chapter 2.2.5.2 --- Method --- p.37 / Chapter 2.2.5.2.1 --- Oil Red O staining --- p.37 / Chapter 2.2.6 --- Determination of triglyceride-protein assay of differentiated PPARβ (+/+) and PPARβ (-/-) MEFs --- p.37 / Chapter 2.2.6.1 --- Materials --- p.39 / Chapter 2.2.6.2 --- Methods --- p.39 / Chapter 2.2.6.2.1 --- Lysis of differentiated MEFs --- p.39 / Chapter 2.2.6.2.2 --- Measurement of triglyceride concentration in cell lysate --- p.40 / Chapter 2.2.6.2.3 --- Measurement of protein concentration in cell lysate --- p.41 / Chapter 2.2.7 --- Preparation of PPARβ(+/+) and PPARβ (-/-) MEF RNA for RT-PCR and Northern blot analysis --- p.42 / Chapter 2.2.7.1 --- Materials --- p.42 / Chapter 2.2.7.2 --- Method --- p.42 / Chapter 2.2.7.2.1 --- RNA isolation --- p.42 / Chapter 2.2.8 --- RT-PCR analysis of differentiated PPARβ(+/+) and PPARβ (-/-) MEFs --- p.44 / Chapter 2.2.8.1 --- Materials --- p.45 / Chapter 2.2.8.2 --- Methods --- p.45 / Chapter 2.2.8.2.1 --- Primer design --- p.45 / Chapter 2.2.8.2.2 --- RT-PCR --- p.46 / Chapter 2.2.9 --- Northern blot analysis of differentiated PPARβ(+/+) and PPARβ (-/-) MEFs --- p.47 / Chapter 2.2.9.1 --- Materials --- p.48 / Chapter 2.2.9.2 --- Methods --- p.49 / Chapter 2.2.9.2.1 --- Preparation of cDNA probes for Northern blotting --- p.49 / Chapter 2.2.9.2.1.1 --- RNA extraction --- p.49 / Chapter 2.2.9.2.1.2 --- Primer design --- p.49 / Chapter 2.2.9.2.1.3 --- RT-PCR of extracted mRNA --- p.50 / Chapter 2.2.9.2.1.4 --- Subcloning of amplified cDNA products --- p.50 / Chapter 2.2.9.2.1.5 --- Screening of recombinant clones by phenol-chloroform extraction --- p.51 / Chapter 2.2.9.2.1.6 --- Confirmation of the recombinant clones by restriction enzyme site mapping --- p.52 / Chapter 2.2.9.2.1.7 --- Confirmation of the recombinant clones by PCR method --- p.52 / Chapter 2.2.9.2.1.8 --- Mini-preparation of plasmid DNA from the selected recombinant clones --- p.54 / Chapter 2.2.9.2.1.9 --- Preparation of cDNA probes --- p.54 / Chapter 2.2.9.2.1.10 --- Formaldehyde agarose gel electrophoresis of RNA --- p.55 / Chapter 2.2.9.2.1.11 --- Hybridization and color development --- p.56 / Chapter 2.3 --- Results --- p.58 / Chapter 2.3.1 --- Confirmation of PPARβ(+/+) and PPARβ (-/-) MEFs genotypes --- p.58 / Chapter 2.3.2 --- PPARβ (-/-) MEFs differentiated similarly to PPARβ(+/+) MEFs as measured by Oil Red O staining --- p.61 / Chapter 2.3.3 --- PPARβ (-/-) MEFs differentiated similarly to PPARβ(+/+) MEFs as reflected by their intracellular triglyceride contents --- p.64 / Chapter 2.3.4 --- PPARβ(-/-) MEFs expressed the adipocyte differentiation marker genes similarly to PPARβ (+/+) MEFs --- p.66 / Chapter 2.4 --- Discussion --- p.77 / Chapter Chapter 3 --- Role of PPARβ in adipocyte differentiation and lipid homeostasis - an in vivo study --- p.82 / Chapter 3.1 --- Introduction --- p.83 / Chapter 3.2 --- Materials and Methods --- p.85 / Chapter 3.2.1 --- Animal and high fat diet treatment --- p.85 / Chapter 3.2.1.1 --- Materials --- p.85 / Chapter 3.2.1.2 --- Method --- p.86 / Chapter 3.2.1.2.1 --- Animal treatment --- p.86 / Chapter 3.2.2 --- Tail-genotyping of PPARβ (+/+) and PPARβ (-/-) mice --- p.87 / Chapter 3.2.2.1 --- Materials --- p.87 / Chapter 3.2.2.2 --- Methods --- p.88 / Chapter 3.2.2.2.1 --- DNA extraction from tail --- p.88 / Chapter 3.2.2.2.2 --- PCR tail-genotyping --- p.89 / Chapter 3.2.3 --- "Measurement of serum triglyceride, cholesterol and glucose levels by enzymatic and spectrophometric methods" --- p.89 / Chapter 3.2.3.1 --- Materials --- p.90 / Chapter 3.2.3.2 --- Methods --- p.91 / Chapter 3.2.3.2.1 --- Serum preparation --- p.91 / Chapter 3.2.3.2.2 --- Measurement of serum triglycerides --- p.91 / Chapter 3.2.3.2.3 --- Measurement of serum cholesterol --- p.92 / Chapter 3.2.3.2.3 --- Measurement of serum glucose --- p.93 / Chapter 3.2.4 --- Measurement of serum insulin and leptin levels by ELISA --- p.94 / Chapter 3.2.4.1 --- Materials --- p.95 / Chapter 3.2.4.2 --- Methods --- p.95 / Chapter 3.2.4.2.1 --- Measurement of serum insulin --- p.95 / Chapter 3.2.4.2.2 --- Measurement of serum leptin --- p.97 / Chapter 3.2.5 --- "Histological studies of liver, interscapular BF and gonadal WF pads" --- p.99 / Chapter 3.2.5.1 --- Materials --- p.100 / Chapter 3.2.5.2 --- Methods --- p.100 / Chapter 3.2.5.2.1 --- "Fixation, dehydration, embedding in paraffin and sectioning" --- p.100 / Chapter 3.2.5.2.2 --- H&E staining --- p.101 / Chapter 3.2.6 --- Analyses of fecal lipid contents --- p.102 / Chapter 3.2.6.1 --- Materials --- p.102 / Chapter 3.2.6.2 --- Method --- p.103 / Chapter 3.2.6.2.1 --- Extraction of lipid contents from stools --- p.103 / Chapter 3.2.7 --- Statistical analysis --- p.104 / Chapter 3.3 --- Results --- p.105 / Chapter 3.3.1 --- Confirmation of genotypes by PCR --- p.105 / Chapter 3.3.2 --- PPARβ (-/-) mice were more resistant to high fat diet-induced obesity --- p.105 / Chapter 3.3.3 --- PPARβ (-/-) mice consumed similarly as to PPARβ (+/+) counterparts… --- p.122 / Chapter 3.3.4 --- Effect of high fat diet on organ weights --- p.128 / Chapter 3.3.4.1 --- PPARβ (-/-) mice were more resistant to high fat diet-induced liver hepatomegaly --- p.134 / Chapter 3.3.4.2 --- PPARβ (-/-) mice were resistant to high fat diet-induced increased white fat depots --- p.134 / Chapter 3.3.4.3 --- PPARβ (-/-) mice were resistant to high fat diet-induced increased brown fat mass --- p.137 / Chapter 3.3.5 --- Effect of high fat diet on organ histology --- p.142 / Chapter 3.3.5.1 --- PPARβ(-/-) mice were more resistant to high fat diet-induced liver steatosis --- p.143 / Chapter 3.3.5.2 --- No defect in white adipocyte expansion in PPARβ(-/-) mice upon high fat diet feeding --- p.153 / Chapter 3.3.5.3 --- No defect in brown adipocyte expansion in PPARβ (-/-) mice upon high fat diet feeding --- p.159 / Chapter 3.3.6 --- "Effect on high fat diet on serum cholesterol, triglyceride, glucose, insulin and leptin levels" --- p.164 / Chapter 3.3.6.1 --- "PPARβ (-/-) mice had a lower serum cholesterol level, but a similar triglyceride level as compared to PPARβ (+/+) mice upon high fat diet feeding" --- p.165 / Chapter 3.3.6.2 --- PPARβ (-/-) mice were resistant to high fat diet-induced insulin resistance --- p.167 / Chapter 3.3.6.3 --- PPARβ (-/-) mice had a similar serum leptin level as PPARβ (+/+) mice --- p.170 / Chapter 3.3.7 --- No decision made in fecal lipid content of PPARβ (+/+) and PPARβ (-/-) mice --- p.173 / Chapter 3.4 --- Discussion --- p.176 / References --- p.182 / Appendices --- p.190

Obesity has been related to a greater incidence of more aggressive, advanced stage prostate cancer. It is expected that serum adipokines related to obesity will promote a more aggressive phenotype in PC cells in vitro. Patient serum (n = 80) was obtained for analysis and divided into four patient groups based on obesity and prostate cancer status. Characteristics of serum-treated PC cells in vitro were measured. In a separate set of analyses, LNCaP and PC3 cells were treated with adiponectin and resistin in vitro, and cell characteristics were analyzed. Serum from obese PC patients induces greater amounts of cell migration and lower amounts of cell proliferation and invasion in vitro. Exogenous treatment of adiponectin on PC cells in vitro does not affect cell migration or invasion. However, adiponectin modulates cytosolic protein levels of soluble β-catenin and GSK-3β, indicating that its mechanism of action may be through the Wnt signalling pathway.