Introduction: In Sweden, 450,000 people suffer from diabetes, of which 10-15% have type 1 diabetes. Individuals who have lived with the disease for a long time run the risk of complications. Physical activity is central to the treatment, but there are risks and obstacles that can lead to the individual avoiding physical activity.  Aim: The purpose is to investigate perceived risks and other obstacles during physical activity for type 1 diabetics.  Methods: The choice of method was a systematic literature study. The databases WorldCat Discovery and Pubmed were used in the search of reports. After the search, 10 reports were selected, and a thematic analysis was applied. Then 3 themes were chosen which were later used to analyze the reports. They were as follows: the fear and the risk of hypoglycemia, the obstacles and remedies in relation to physical activity and behavioral changes in the individual.  Results: The fear of a hypoglycemia prevents the individual from exercising. The result showed that women suffers from anxiety concerning their diabetes to a greater extent than men. Aids such as Continuous Glucose Monitoring can minimize anxiety and the risk of getting into hypoglycemia during physical activity.  Conclusion: Constantly worrying about getting into hypoglycemia can cause the individual to stop caring for the risks associated with the disease. One of the factors that led to the individual being unable to perform physical activity was hyperglycaemia. Continuous blood glucose monitoring as well as support of personnel at exercise facilities can lead to the individual overcoming obstacles and concerns.

Thesis (M.Ing. (Mechanical Engineering))--North-West University, Potchefstroom Campus, 2007.

Type 1 Diabetes is a dangerous and life-long disease for which its prevalence is global. Research has shown that tight glycaemic control of this disease significantly reduces the risks of developing several life threatening diabetic complications. The Ets-Insulin-Bolus Calculator (EIBC), inspired by the Ets concept (Equivalent Teaspoon Sugar), was primarily designed to assist type I diabetics in improving their blood glucose control. The EIBC has shown to improve the average blood glucose level of type 1 diabetics. The need for this study however is to determine whether the ET!3C promotes tighter glycaemic control for type 1 diabetics based on a more-in-depth numerical analysis. With the use of the latest technology in blood glucose monitoring, the CGMS from Medtronic, mathematical models expressing and rating blood glucose control have been proposed and derived in this study. A clinical trial with type 1 diabetics has also been conducted. The use of the models together with the clinical trial results have shown that the EIBC does in fact promote tighter glycaemic control for type 1 diabetics. / Thesis (M.Ing. (Mechanical Engineering))--North-West University, Potchefstroom Campus, 2007.

Type 1 Diabetes is a dangerous and life-long disease for which its prevalence is global. Research has shown that tight glycaemic control of this disease significantly reduces the risks of developing several life threatening diabetic complications. The Ets-Insulin-Bolus Calculator (EIBC), inspired by the Ets concept (Equivalent Teaspoon Sugar), was primarily designed to assist type I diabetics in improving their blood glucose control. The EIBC has shown to improve the average blood glucose level of type 1 diabetics. The need for this study however is to determine whether the ET!3C promotes tighter glycaemic control for type 1 diabetics based on a more-in-depth numerical analysis. With the use of the latest technology in blood glucose monitoring, the CGMS from Medtronic, mathematical models expressing and rating blood glucose control have been proposed and derived in this study. A clinical trial with type 1 diabetics has also been conducted. The use of the models together with the clinical trial results have shown that the EIBC does in fact promote tighter glycaemic control for type 1 diabetics. / Thesis (M.Ing. (Mechanical Engineering))--North-West University, Potchefstroom Campus, 2007.

Yes / Aims/hypothesis Hypoglycaemia is a major barrier to good glucose control in type 1 diabetes. Frequent hypoglycaemic episodes impair awareness of subsequent hypoglycaemic bouts. Neural changes underpinning awareness of hypoglycaemia are poorly defined and molecular mechanisms by which glial cells contribute to hypoglycaemia sensing and glucose counterregulation require further investigation. The aim of the current study was to examine whether, and by what mechanism, human primary astrocyte (HPA) function was altered by acute and recurrent low glucose (RLG). Methods To test whether glia, specifically astrocytes, could detect changes in glucose, we utilised HPA and U373 astrocytoma cells and exposed them to RLG in vitro. This allowed measurement, with high specificity and sensitivity, of RLG-associated changes in cellular metabolism. We examined changes in protein phosphorylation/expression using western blotting. Metabolic function was assessed using a Seahorse extracellular flux analyser. Immunofluorescent imaging was used to examine cell morphology and enzymatic assays were used to measure lactate release, glycogen content, intracellular ATP and nucleotide ratios. Results AMP-activated protein kinase (AMPK) was activated over a pathophysiologically relevant glucose concentration range. RLG produced an increased dependency on fatty acid oxidation for basal mitochondrial metabolism and exhibited hallmarks of mitochondrial stress, including increased proton leak and reduced coupling efficiency. Relative to glucose availability, lactate release increased during low glucose but this was not modified by RLG. Basal glucose uptake was not modified by RLG and glycogen levels were similar in control and RLG-treated cells. Mitochondrial adaptations to RLG were partially recovered by maintaining euglycaemic levels of glucose following RLG exposure. Conclusions/interpretation Taken together, these data indicate that HPA mitochondria are altered following RLG, with a metabolic switch towards increased fatty acid oxidation, suggesting glial adaptations to RLG involve altered mitochondrial metabolism that could contribute to defective glucose counterregulation to hypoglycaemia in diabetes. / Diabetes UK (RD Lawrence Fellowship to CB; 13/0004647); the Medical Research Council (MR/N012763/1) to KLJE, ADR and CB; and a Mary Kinross Charitable Trust PhD studentship to CB, ADR and RW to support PGWP. Additional support for this work came from awards from the British Society for Neuroendocrinology (to CB and KLJE), the Society for Endocrinology (CB), Tenovus Scotland (CB) and the University of Exeter Medical School (CB and KLJE). AR was also supported by a Royal Society Industry Fellowship.

Le maintien de notre poids corporel résulte d'un équilibre entre les dépenses et les apports énergétiques. Cet équilibre appelé « homéostasie énergétique » implique un grand nombre de molécules. Parmi elles, la nesfatine-1, découverte en 2006, est un peptide de 82 acides aminés issu du clivage de la protéine NUCB2. L'intérêt généré par la nesfatine-1 réside dans son action anorexigène exercée indépendamment de la signalisation à la leptine. La nesfatine-1 est exprimée dans plusieurs organes tels que le tissu adipeux, l'estomac, le pancréas, ainsi que le cerveau. Dans le cerveau, son expression se limite principalement à quelques groupes neuronaux localisés dans l'hypothalamus et le complexe vagal dorsal. Au cours de ce travail, nous avons analysé la sensibilité des neurones exprimant NUCB2/nesfatine-1 aux signaux périphériques physiologiques et physiopathologiques affectant la prise alimentaire. Nous montrons que ces neurones sont sensibles à une hypoglycémie et qu'ils pourraient contribuer à la contre-régulation mise en place afin de rétablir la glycémie de base. De plus, nous montrons qu'ils sont activés en réponse à deux stimuli inflammatoires : l'administration de lipopolysaccharide et l'intoxication alimentaire avec une mycotoxine appelée déoxynivalénol. Ainsi, les neurones exprimant NUCB2/nesfatine-1 pourraient contribuer au développement de l'anorexie inflammatoire. Cette étude a constitué la première mise en évidence d'une implication de ce peptide en situation pathologique. L'ensemble de ces résultats suggère qu'en plus de son effet satiétogène, la nesfatine-1 participe à la signalisation centrale impliquée dans la glucodétection et les réponses inflammatoires. / The long term maintenance of body weight results from a balance between energy expenditure and intake. This balance, called “energy homeostasis”, involves a large number of molecules. Among these, nesfatin-1, discovered in 2006, is an 82 amino-acid peptide derived from the cleavage of the protein NUCB2. The interest generated by nesfatin-1 lies in its anorexigenic effect performed independently of leptin signalization. Nesfatin-1 is expressed in several organs such as adipose tissue, stomach, pancreas, and brain. In the brain, its expression is limited to a few neuronal groups located in the hypothalamus and dorsal vagal complex. In this work, we analyzed the sensitivity of NUCB2/nesfatin-1-expressing neurons to physiological and physiopathological peripheral signals affecting food intake. We show that these neurons are sensitive to hypoglycemia and that they could contribute to the counter-regulatory response established in order to restore the basal blood glucose level. Moreover, we show that they are activated in response to two inflammatory stimuli: lipopolysaccharide administration and food intoxication with a mycotoxin named deoxynivalenol. So, NUCB2/nesfatin-1-expressing neurons could contribute to the development of inflammatory anorexia. This study was the first evidence of an involvement of this peptide in a pathological situation. Taken together, these results suggest that in addition to its satiating effect, nesfatin-1 participates in the central signalization involved in glucodetection and inflammatory responses.

Exercise has a wide range of benefits for patients with type 1 diabetes, including improvements in body composition, cardiovascular risk profile and glycaemic control. Unfortunately, exercise also increases the risk of hypoglycaemia in children with type 1 diabetes, both at the time of exercise and for many hours afterwards. The availability of clear, evidence-based guidelines regarding appropriate adjustments in carbohydrate intake or insulin doses may help to prevent this exercise associated hypoglycaemia. However, current guidelines regarding exercise in children with type 1 diabetes rely heavily on adult literature or the consensus of experts. Therefore, further studies are needed in young people with diabetes to document the metabolic responses during and following exercise. In particular, the mechanisms underlying hypoglycaemia occurring many hours after exercise require further exploration. In addition, as children often exercise in the afternoon, studies performed at this time of the day are more likely to be transferrable to a real life situation. For this reason, we studied adolescents with type 1 diabetes to investigate physiological responses to exercise, focusing on afternoon activity and employing a novel variation of the euglycaemic insulin clamp technique. The core experiments involved studying diabetic adolescents on two occasions in a counterbalanced, paired design during and after afternoon exercise. Insulin was infused at a constant rate based on the subjects' usual daily insulin dose and glucose was infused to maintain euglycaemia. At 1600 hrs subjects either exercised at a moderate intensity (95% of their lactate threshold) for 45 minutes on a cycle ergometer (exercise study), or sat on the ergometer without exercising (rest study). Using this experimental design, it was found that glucose infusion rates (GIR) to maintain euglycaemia were elevated during and shortly following exercise and again from 7-11 hours after exercise compared with the rest study. Counterregulatory hormone levels were similar between the exercise and rest studies except for peaks in noradrenaline, cortisol and growth hormone levels at the end of exercise. Glucagon and adrenaline levels did not increase with exercise. The observed biphasic increase in glucose requirements paralleled the observed clinical risk of hypoglycaemia immediately during exercise and the delayed risk of hypoglycaemia which often occurs overnight.

No description available.

Background: Changing service demands require United Kingdom ambulance services to redefine their role and response strategies, in order to reduce unnecessary Emergency Department attendances. Treat and Refer guidelines have been developed with this aim in mind. However, these guidelines have been developed in the absence of reliable evidence or guiding mid-range theory. This has resulted in inconsistencies in clinical practice. One condition frequently included in Treat and Refer guidelines is hypoglycaemia. Therefore this thesis aimed to investigate prehospital hypoglycaemic emergencies in order to develop an evidence base for future interventions and guideline development. Research approach: A pragmatic and inductive applied health services research approach was employed. Multiple methods were used in a sequential explanatory design. Three linked studies were undertaken with the results of previous studies informing the development of the next. Study one: A scoping review of prehospital treatment of hypoglycaemic events. Aims: i) To describe the demographics of the patient population requiring ambulance service assistance for hypoglycaemic emergencies; ii) To determine the extent to which post-hypoglycaemic patients with diabetes, who are prescribed oral hypoglycaemic agents (OHA), experience repeat hypoglycaemic events (RHE) after being treated in the prehospital environment. Methods: A scoping literature review was conducted using an overlapping retrieval strategy that included both published and unpublished literature. Findings: Twenty-three papers and other relevant material were included. Hypoglycaemia related ambulance calls account for 1.3% to 5.2% of ambulance calls internationally. Transportation rates varied between studies (25%-73%). Repeat hypoglycaemic emergencies are experienced by 2-7% of patients within 48 hours. There was insufficient detail to determine any relationship between repeat events and OHA. The low quality of included papers means that the results should be cautiously interpreted. The safety of leaving patients on OHA at home post hypoglycaemic emergency is unknown. Consequently patients taking OHAs who experience a hypoglycaemic emergency should be transported to hospital for observation. There was a lack of knowledge about the Scottish demographics of the patient population. Study two: A retrospective cross-sectional observational study of diabetes related emergency calls. Aims: To investigate i) the patient demographics and characteristics of hypoglycaemia related emergency calls; ii) the incidence of repeat hypoglycaemic events; and iii) the factors associated with emergency calls that result in individuals being left at home. Methods: A retrospective observational cross-sectional study conducted using Medical Priority Dispatch System® call data from West of Scotland Ambulance Control Centre over a 12 month period. Data were extracted on age, gender, dispatch code, time of call, deprivation category, and immediate outcome (home or hospital). Multiple regression analysis was used to determine predictors of remaining at home. Findings: 1319 calls for hypoglycaemia were received. Patient demographics were similar to the scoping review findings. Most patients remained at home (N = 916 vs N = 380; p < .001). RHE’s were experience by 3.1% within 48 hours, and 10.6% within two weeks. The most significant independent predictor for patients remaining at home was a prior call to the ambulance service (OR of 2.4 [95%CI 1.5 to 3.7]). Patients’ reasons for remaining at home and the causes of subsequent severe events are unknown. It is likely that non-clinical factors may explain some of this behaviour. Study 3: Investigating patients’ experiences of prehospital hypoglycaemic care. Aim: To investigate the experiences of patients who are attended by ambulance clinicians for a hypoglycaemic emergency. Methods: In-depth interviews with adults with diabetes who had recently experienced a hypoglycaemic emergency treated by ambulance clinicians. Participants were recruited from Greater Glasgow and Clyde and Lanarkshire Health Board areas. Data were analysed using Framework Analysis. Findings: Twenty six patients were interviewed. Three key themes were developed. Firstly, an explanation for help seeking behaviour; patients’ impaired awareness of hypoglycaemia as well as the inability of friends and relatives to cope can contribute to an ambulance call-out. Secondly, the perceptions of ambulance service care; patients felt the service provided was good; however ambulance clinicians’ advice was inconsistent. Thirdly, the influences on uptake of follow-up care; patient preferences for follow-up care were influenced by previous experiences of home, hospital and primary care. Post-hoc analysis identified three psychological theories that may explain these findings and provide a useful basis for intervention development: Common Sense Model (Leventhal et al, 1998); Health Belief Model (Rosenstock, 1966); Ley’s cognitive hypothesis model of communication (Ley and Llewelyn, 1995; 1981). Conclusion: Most people treated for severe hypoglycaemia by ambulance clinicians remain at home and do not follow-up their care. A few experience repeat hypoglycaemic emergencies. Key causal, but modifiable factors, contributing to this include:- impaired awareness of hypoglycaemia; inconsistent delivery of ambulance clinician referral advice; and patients’ perceptions of the costs and benefits of follow-up care. Ambulance services cannot address all these factors in isolation. The studies in this thesis have generated an evidence base and identified plausible candidate theories. This will support the future development of novel interventions to improve severe hypoglycaemic emergency follow-up.

No description available.