Thesis (M.N.)--Memorial University of Newfoundland, 2004. / Typescript. Bibliography: leaves 141-150.

Diabetes typ 1 och 2 är idag en folksjukdom och antalet nyinsjuknade ökar i samma omfattning som fetmaepidemin. Dess behandling är emellertid komplex varför föreliggande litteraturstudie syftade till att beskriva vuxna individers erfarenheter av att leva med diabetes typ 1 och 2. Litteratursökningen utfördes i databaserna CINAHL och PubMed. Både kvantitativa och kvalitativa studier (N=10) inkluderades vilka kvalitetsgranskades av båda författarna oberoende av varandra med hjälp av ett modifierat granskningsprotokoll. Resultatet visade att individernas erfarenheter av att leva med sjukdomen berörde sex olika teman; plasmaglukosnivån, copingstrategier, insulinpump/insulinpenna/antidiabetikum, kost, stöd och oro. Individer med diabetes typ 1 eller 2 upplevde att de oftast fick för lite information angående sjukdomen varför deras oro över akuta- och senkomplikationer ökade. Kosthållningen beskrevs också svår och problemfylld när övriga familjemedlemmar motsatte sig denna. Individerna betonade därför vikten av stöd från familj och anhöriga.Nyckelord: Diabetes Mellitus typ 1, diabetes mellitus typ 2, erfarenhet, litteraturstudie, omvårdnad / Today, diabetes type 1 and 2 are seen as a public health issue, and the number of newly diagnosed are increasing to the extent of obesity. The treatment is, however, complex why the literature review presented aims at describing adult individuals experience about living with diabetes type 1 and 2. The literature search was performed in the databases CINAHL and PubMed. Both quantitative and qualitative studies (N=10) were included, and quality rated, by both authors independently of each others, by means of a modified review record. The result showed that individuals experience about living with diabetes type 1 and 2 concerned six different themes: plasma glucose level, coping strategies, insulin pump/insulin pen/antidiabeticum, diet, support and anxiety. Individuals diagnosed with diabetes type 1 or 2 experienced that they didn’t receive enough information regarding the disease, which resulted in worries aboute acute- and late- complications. A majority experienced the diet restrictions as difficult and troublesome because the family opposed the new diet. The individuals experienced that support from the family and relatives were important, but a balance was an aim. Keywords: Diabetes Mellitus type 1, diabetes mellitus type 2, experiences, nursing, review

Lic.-avh. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 2 uppsatser.

Diss. (sammanfattning) Linköping : Univ., 2004. / Härtill 5 uppsatser.

Hypertension and type two diabetes mellitus (Type 2 DM) are serious chronic illnesses that impact on the lives of millions of people around the world. Various epidemiological studies have shown a relationship between early life events such as intrauterine growth retardation (IUGR) resulting in low birth weight and the development of these chronic illnesses in adult life. To explain the link between these two events, it has been suggested that an ‘insult’ at a critical time point of development can ‘program’ alterations in gene expression, organ size, and cell number. This has been termed “the early life origins of disease’. There is also evidence that these programmed effects are not limited to the first generation but can also be passed to subsequent generations. With changes in lifestyle in modern society, the prevalence of obesity is increasing, in association with problems such as type 2 DM, hypertension, fatty liver, atherosclerosis and the metabolic syndrome. Obesity during pregnancy is linked to problems such as gestational diabetes, hypertension and early miscarriage as well as a higher risk of congenital malformations. Maternal obesity has also been recognised as one of the factors capable of ‘programming’ the offspring, increasing the risk of childhood and adult disorders such as obesity and hypertension. In this thesis I have used two animal models to explore the underlying mechanisms of programming and its intergenerational effects: i) a rat model of prenatal glucocorticoid over-exposure (the dexamethasone-programmed rat) and ii) a mouse model of obesity during pregnancy. Using the dexamethasone-programmed rat, I have shown that prenatal glucocorticoid overexposure reduces fetal and placental weight in the first generation (F1) offspring, in association with alterations in gene expression in placenta and liver. In addition, I have shown effects on fetal and placental weights and gene expression in the second generation (F2) offspring. The observed changes in gene expression in the F2 offspring differ from those in the first generation. Thus, although effects on fetal growth are seen in both generations, the underlying mechanisms appear to be different. We also observed marked parent of origin effects on fetal and placental growth and gene expression in the second generation. In the mouse model of maternal obesity, birth weight was decreased in the F1 offspring. At weaning, the offspring of obese mothers were heavier than controls, however this difference in weight was not persistent. At three months of age, F1 female offspring of obese mothers showed altered expression of hepatic genes important in lipid regulation and metabolism. More striking changes were seen in the F2 generation in which there was an effect of paternal exposure to maternal obesity to decrease birth weight. There were also parent of origin effects on organ weights and insulin levels at six months of age. These results provide evidence for the transmission of programming effects to a second generation in two different programming models and suggest that the mechanisms leading to these effects differ between generations.

Bakgrund: Diabetes mellitus typ 1 är en autoimmun sjukdom och antalet som insjuknar ökar varje år. Under ungdomstiden sker mycket i människans kropp och det kan vara en utmaning att balansera blodsockernivåer när hormonerna i kroppen svajar. Ungdomar med diabetes mellitus typ 1 står därför inför stora utmaningar för att lyckas med sin behandling. Syfte: Syftet är att belysa ungdomars upplevelser av att leva med diabetes mellitus typ 1. Metod: Metoden är en litteraturstudie baserad på både kvalitiva och kvantitativa studier. Analysen är genomförd utifrån en modell av Axelsson (2012). Resultat: I resultatet framkom att ungdomarna med diabetes mellitus typ 1 växte in i rollen i att bli mer självständiga i sin behandling. Detta var inte alltid lätt. Ungdomarna påverkades av hur deras vänner bemötte diagnosen, hur de blev bemötta av vården samt hur villiga deras föräldrar var att lämna över ansvaret. Resultatet presenteras utifrån fyra huvudteman samt nio subteman. Diskussion:I diskussionen tar vi upp vikten av att jobba med målet att patienten ska få kunskap så att denne kan sköta sin behandling självständigt. Vikten av stöd för att motverka känslor av skam för sjukdomen och dess behandling belyses också.

Diabetes mellitus typ 1 är en autoimmun sjukdom, vilket innebär att immunsystemet ser betacellerna i bukspottskörteln som främmande och angriper dem. Cellerna kan då inte producera insulin längre, vilket är ett livsviktigt hormon för kroppen. I Sverige insjuknar cirka två barn varje dag i diabetes mellitus typ 1. Sjukdomen påverkar barnets vardag och kommer alltid vara en styrande del genom livet. Många barn oroar sig över hypoglykemi samt andra komplikationer som är relaterade till sjukdomen. Syftet med studien är att beskriva upplevelser av hur vardagen påverkats hos barn som är diagnostiserade med diabetes mellitus typ 1. Metoden är en sammanställning av empirisk data och baseras utifrån Axelssons (2012) modell. Studien innehåller 11 artiklar som består av både kvalitativa och kvantitativa ansatser. Examensarbetet fokuserar på barn i åldern 6-14 år och artiklarna i studien belyser upplevelsen av att leva med diabetes mellitus typ 1. Resultatet visade att barnen upplevde känslor av utanförskap och att de kände sig annorlunda jämfört med sina vänner. Familjen hade en betydelsefull roll för barnen och sjukdomen påverkade även omgivningen. Resultatet presenteras utifrån fyra huvudkategorier och tio subkategorier. I diskussionen belyser vi känslan av att vara barn och leva med en kronisk sjukdom, familjens betydelse samt att förlika sig med sjukdomen. En grundläggande aspekt som framkommer i diskussionen är även vikten av adekvat och individanpassad information efter barnets utvecklingsnivå.

Type 2 diabetes (T2D) is a metabolic disease that results from complex interactions between the environment, the genetic variation and epigenetic regulation of gene expression in individuals. Beta-cell dysfunction and insulin resistance are regarded as the hallmarks of the disease as the common presentation of T2D is the inability of beta-cells to adequately respond to the insulin demands of the body. The prevalence of T2D in Africa, and particularly South Africa, is on the rise. This is very likely the result of the combination of genetic susceptibility with increasing availability and accessibility of relatively cheap, highly palatable, calorie-dense meals with no corresponding lifestyle adjustment. This study aims to utilize available data from GWAS and gene expression arrays to identify potential variants that likely influence T2D susceptibility in African populations. Two public data repositories were mined – the National Center for Biotechnology Information’s (NCBI) Gene Expression Omnibus (GEO) and the National Human Genome Research Institute’s (NHGRI) GWAS Catalog. The criteria for selecting the studies for inclusion were based on ten descriptive T2D-related terms taken from the GWAS catalog’s pre-defined search categories. These terms were also applied to the selection of gene expression studies in GEO. These terms are: “fasting glucose-related traits”, “fasting insulin-related traits”, “fasting plasma glucose”, “insulin resistance/response”, “insulin traits”, “diabetes-related insulin traits”, “pro insulin levels” “Type 2 diabetes”, “type 2 diabetes and 6 quantitative traits” and “type 2 diabetes and other traits”. Ten Affymetrix platform-based studies in human tissues were chosen from GEO using these criteria. A Benjamin-Hochberg adjusted p-value of 0.05 was set as a cut-off for significant differentially expressed genes (7,887 genes) with 497 genes occurring in two or more studies, based on tissue- or array-type, considered candidates for downstream analysis. The GWAS catalogue presented 175 “reported” genes and 218 SNPs from 51 studies matching the set T2D-related criteria. Functional analyses done with the Database for Annotation, Visualization and Integrated Discovery (DAVID) on both the GWAS and expression studies genes lists,

by Mui Kin Tung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1993. / Includes bibliographical references (leaves 97-113). / Chapter CHAPTER 1: --- INTRODUCTION --- p.1 / Chapter CHAPTER 2: --- LITERATURE REVIEW --- p.5 / Chapter 2.1 --- ION TRANSPORT SYSTEMS IN HUMAN ERYTHROCYTES --- p.6 / Chapter 2.1.1 --- "Sodium Pump (Na+,K+-ATPase)" --- p.6 / Chapter 2.1.2 --- Passive Sodium Transport Systems --- p.9 / Chapter 2.1.2.1 --- Sodium-potassium-chloride cotransport system --- p.9 / Chapter 2.1.2.2 --- Sodium-lithium Countertransport --- p.13 / Chapter 2.1.3 --- Ouabain- and Frusemide-Resistant Passive Effluxes --- p.17 / Chapter 2.2 --- ERYTHROCYTE SODIUM TRANSPORT SYSTEMS IN ESSENTIAL HYPERTENSION --- p.17 / Chapter 2.2.1 --- "Sodium Pump (Na+, K+-ATPase) in Essential Hypertension" --- p.18 / Chapter 2.2.2 --- Sodium-Potassium-Chloride Cotransport in Essential Hypertension --- p.20 / Chapter 2.2.3 --- Sodium-Lithium Countertransport in Essential Hypertension --- p.23 / Chapter 2.2.4 --- Passive Ion Fluxes in Essential Hypertension --- p.26 / Chapter 2.2.5 --- Intracellular Sodium Concentration in Essential Hypertension --- p.26 / Chapter 2.3 --- ERYTHROCYTE SODIUM TRANSPORT SYSTEMS IN DIABETES MELLITUS --- p.27 / Chapter CHAPTER 3: --- MATERIALS & METHODS --- p.29 / Chapter 3.1 --- MATERIALS --- p.30 / Chapter 3.1.1 --- Choline Wash Solution (CWS) --- p.30 / Chapter 3.1.2 --- Lithium Loading Solution --- p.31 / Chapter 3.1.3 --- Choline Wash Solution with Ouabain (CWS-O) --- p.31 / Chapter 3.1.4 --- Sodium Containing Medium (SCM) --- p.31 / Chapter 3.1.5 --- Sodium Free Medium (SFM) --- p.31 / Chapter 3.1.6 --- Sodium Free Medium with Bumetanide (SFM-B) --- p.32 / Chapter 3.1.7 --- Preservation Solution --- p.32 / Chapter 3.2 --- STUDY POPULATION --- p.32 / Chapter 3.2.1 --- Control Subjects --- p.35 / Chapter 3.2.2 --- Patients with Essential Hypertension --- p.35 / Chapter 3.2.3 --- Diabetic Patients --- p.35 / Chapter 3.3 --- DETERMINATION OF ERYTHROCYTE INTRACELLULAR SODIUM AND POTASSIUM CONCENTRATIONS (Naic/Kic --- p.36 / Chapter 3.3.1 --- Preparation of Erythrocytes --- p.36 / Chapter 3.3.2 --- Preparation of Haemolysates --- p.38 / Chapter 3.3.3 --- Determination of Sodium and Potassium Concentrations in Haemolysates --- p.38 / Chapter 3.3.4 --- Determination of Haemoglobin Concentration in Haemolysates --- p.38 / Chapter 3.3.5 --- Evaluation of Erythrocyte Intracellular Sodium and Potassium Concentrations --- p.39 / Chapter 3.4 --- DETERMINATION OF ERYTHROCYTE PASSIVE POTASSIUM EFFLUX --- p.39 / Chapter 3.4.1 --- Determination of Potassium Concentrations in Supernatant --- p.40 / Chapter 3.4.2 --- Evaluation of Passive Potassium Efflux --- p.40 / Chapter 3.5 --- DETERMINATION OF ERYTHROCYTE SODIUM-LITHIUM COUNTERTRANSPORT (SLC) AND LITHIUM-POTASSIUM COTRANSPORT (LPC) --- p.41 / Chapter 3.5.1 --- Lithium Loading --- p.42 / Chapter 3.5.2 --- Determination of Haematocrit --- p.42 / Chapter 3.5.3 --- Preparation of Haemolysates --- p.42 / Chapter 3.5.4 --- Determination of the Lithium Concentration in Haemolysates --- p.43 / Chapter 3.5.5 --- Determination of Lithium Efflux --- p.43 / Chapter 3.5.6 --- Evaluation of Lithium Efflux Rate --- p.43 / Chapter 3.5.7 --- Evaluation of Intracellular Lithium Concentration --- p.44 / Chapter 3.6 --- VALIDATION OF METHODOLOGY FOR DETERMINATION OF ERYTHROCYTE SODIUM TRANSPORT SYSTEMS --- p.45 / Chapter 3.6.1 --- Effect of Time Course of Lithium Efflux --- p.45 / Chapter 3.6.2 --- Intracellular Potassium Concentration and Its Effect on Ouabain- and Frusemide-Resistant Passive Potassium Efflux --- p.45 / Chapter 3.7 --- PRESERVATION OF ERYTHROCYTES FOR DETERMINATION OF SODIUM TRANSPORT SYSTEMS --- p.51 / Chapter 3.8 --- PRECISION OF THE METHOD --- p.51 / Chapter 3.9 --- STATISTICS --- p.52 / Chapter CHAPTER 4: --- RESULTS --- p.56 / Chapter 4.1 --- POPULATION CHARACTERISTICS --- p.57 / Chapter 4.2 --- ERYTHROCYTE INTRACELLULAR LITHIUM CONCENTRATIONS AFTER LITHIUM LOADING --- p.57 / Chapter 4.3 --- RELATIONSHIP BETWEEN ERYTHROCYTE ION TRANSPORT PARAMETERS AND OTHER VARIABLES --- p.58 / Chapter 4.4 --- ERYTHROCYTE SODIUM TRANSPORT SYSTEMS IN ESSENTIAL HYPERTENSION --- p.64 / Chapter 4.5 --- ERYTHROCYTE SODIUM TRANSPORT SYSTEMS IN PATIENTS WITH DIABETES MELLITUS --- p.64 / Chapter 4.5.1 --- NIDDM Patients without Hypertension --- p.64 / Chapter 4.5.2 --- NIDDM Patients with Hypertension --- p.65 / Chapter 4.5.3 --- NIDDM Patients with and without Hypertension --- p.65 / Chapter 4.6 --- ERYTHROCYTE SODIUM TRANSPORT SYSTEMS IN DIABETES MELLITUS PATIENTS WITH PROTEINURIA --- p.65 / Chapter 4.6.1 --- Clinical Features and Biochemistry Indices --- p.69 / Chapter 4.6.2 --- Ion Transport Systems and NIDDM Patients with Proteinuria --- p.69 / Chapter 4.7 --- EFFECTS OF TREATMENTS ON ERYTHROCYTE ION TRANSPORT SYSTEMS IN DIABETIC HYPERTENSIVE PATIENTS --- p.70 / Chapter 4.7.1 --- Effects of Diuretic Therapy --- p.70 / Chapter 4.7.2 --- Effects of Enalapril and Nifedipine Therapy --- p.74 / Chapter 4.7.3 --- Effects of Enalapril Therapy --- p.74 / Chapter 4.7.4 --- Effects of Nifedipine Therapy --- p.75 / Chapter 4.7.5 --- Comparison of the Effects of Enalapril and Nifedipine Therapy --- p.75 / Chapter CHAPTER 5: --- DISCUSSION --- p.81 / Chapter 5.1 --- SODIUM TRANSPORT IN ESSENTIAL HYPERTENSION --- p.82 / Chapter 5.1.1 --- Erythrocyte Sodium-Lithium Countertransport in Essential Hypertension --- p.82 / Chapter 5.1.2 --- Erythrocyte Sodium-Potassium Cotransport in Essential Hypertension --- p.86 / Chapter 5.1.3 --- Erythrocyte Intracellular Concentration of Sodiumin Essential Hypertension --- p.87 / Chapter 5.1.4 --- Erythrocyte Passive Potassium Efflux in Essential Hypertension --- p.90 / Chapter 5.2 --- SODIUM TRANSPORT SYSTEMS IN NON-INSULIN- DEPENDENT DIABETES MELLITUS (NIDDM) --- p.91 / Chapter 5.2.1 --- Sodium-Lithium Countertransport in Non-Insulin-Dependent Diabetes Mellitus --- p.91 / Chapter 5.2.2 --- Erythrocyte Lithium-Potassium Cotransport and Intracellular Sodium Concentration in Non-Insulin-Dependent Diabetes Mellitus --- p.93 / Chapter 5.3 --- EFFECT OF ANTIHYPERTENSIVE AGENTS ON ERYTHROCYTE SODIUM TRANSPORT SYSTEMS --- p.95 / REFERENCES --- p.98

Type 2 diabetes mellitus affects over 100 million people worldwide. It is characterized by various metabolic abnormalities such as insulin resistance, aberrant insulin secretion, hyperglycaemia and a cluster of cardiovascular risk factors, including increased oxidative stress. It is associated with microvascular complications and increased potential of macrovascular disease. The aim of the studies described in this thesis was to test the hypothesis that oxidant stress contributes to an altered vascular function and impaired insulin regulation in a pre-diabetic animal model- the obese Zucker rats. The first objective was to develop new methods to measure endothelial function in animal disease models. Firstly, without autonomic control - the in situ perfused hindquarters, and secondly, with autonomic control - the in vivo Doppler ear blood flow. The obese Zucker rat was shown to have increased oxidative stress, as measured by plasma 8-epi-PGF2a,. It also had high insulin and glucose levels and impaired glucose disposal. Obese rats also had increased agonist-induced nitric oxide-dependent endothelial responses; these were further enhanced by insulin in a macrovascular preparation, but were impaired by insulin in a resistance vessel bed. Following dietary treatment with the antioxidants, the obese plasma insulin/glucose ratio was improved. However, vitamin E blunted the enhanced endothelial-dependent vasodilator responses, and decreased plasma levels of 8-epi-PGF2a. In contrast, pro-oxidant treatment with hydroquinone and buthionine-sulphoximine impaired the plasma insulin/glucose ratio, abolished endothelial hyperactivity but increased plasma 8-epi-PGF2a levels. Interestingly, fructose protected against pro-oxidant-induced increases in plasma 8-epi-PGF2a levels and further increases in glucose-induced plasma insulin. In summary the redox status in obese Zucker rats was modified with antioxidant and prooxidant treatment. This resulted in compensatory changes in glucose disposal and endothelial function. Impaired endothelial function may initiate "damage" especially in those individuals susceptible to syndrome X, leading to insulin insensitivity and vascular dysfunction in type 2 diabetes.