Abnormal carbohydrate metabolism is a commonly encountered feature of malaria in people, and similar derangements have been detected in veterinary patients with canine babesiosis. Glucose, the major metabolic fuel source, is a key resource in critically ill patients as they mount an immunological response to infection and inflammation. The ability of the individual to effectively mobilise, distribute and utilise glucose is a major determinant of morbidity and mortality. Hypoglycaemia has been identified as a life threatening metabolic complication in almost 20% of severely ill dogs suffering from babesiosis due to Babesia rossi infection. Insulin and glucagon are the primary hormones involved in glucose homeostasis. Insulin lowers blood glucose concentration by facilitating cellular uptake and utilisation of glucose. Hyperinsulinaemia as a result of inappropriate insulin secretion may precipitate hypoglycaemia, and has been identif ed as a cause of hypoglycaemia in human and murine malaria. A similar phenomenon may exist in canine babesiosis. This prospective, cross-sectional, observational study, including 94 dogs with naturally acquired virulent babesiosis, sought to investigate and characterise the relationship between blood glucose concentrations and insulin concentrations in cases of canine babesiosis. Pre-treatment jugular blood samples were collected for simultaneous determination of plasma glucose and insulin concentrations. Animals were retrospectively divided into three groups: hypoglycaemic (plasma glucose concentration < 3.3 mmol/L; n=16), normoglycaemic (3.3-5.5 mmol/L; n=62), and hyperglycaemic (> 5.5 mmol/L; n=16). The median plasma insulin concentrations (IQR in parentheses) for the hypoglycaemic, normoglycaemic and hyperglycaemic groups were 10.7 pmol/L (10.7-18.8 pmol/L), 10.7 pmol/L (10.7-29.53 pmol/L; i.e below the detection limit of the assay), and 21.7 pmol/L (10.7-45.74 pmol/L), respectively. Statistical analysis revealed no significant difference in insulin concentration between the three groups. These results suggest that insulin secretion was appropriately suppressed in these dogs. Only two dogs had elevated insulin concentrations, one of which was hypoglycaemic. The median time since last meal (available for 87 dogs) was 24 hours (IQR 2-4 days), constituting a significant period of illness-induced starvation. We conclude that hyperinsulinaemia is not a cause of hypoglycaemia in virulent canine babesiosis. It is speculated that prolonged fasting due to disease-induced anorexia, in addition to increased glucose consumption, depletion of hepatic glycogen stores, and hepatic dysfunction with impaired gluconeogenesis, may play important roles in the pathophysiology of hypoglycaemia in canine babesiosis. / Dissertation (MMedVet)--University of Pretoria, 2010. / Companion Animal Clinical Studies / unrestricted

Background. Diabetes mellitus (DM) is a common condition. The high burden of undiagnosed DM and lack of large population studies make accurate prevalence estimations difficult, especially in the surgical environment. Furthermore, poorly controlled DM is associated with an increased risk of perioperative complications and mortality. Objectives. The primary objective was to establish the prevalence of DM in elective adult non-cardiac, non-obstetric surgical patients in Western Cape hospitals. The secondary objectives were to assess the glycaemic control and compliance with treatment of known diabetics. Methods. This was a five-day, multicentre, prospective observational study performed at six government-funded hospitals in the Western Cape. Screening for DM was done using fingerprick capillary blood glucose (CBG) testing. Patients found to have a CBG of ≥ 6.5 mmol/L had an HbA1c level done. DM was diagnosed based on the Society for Endocrinology, Metabolism and Diabetes of South Africa (SEMDSA) diagnostic criteria. Patients known with DM had an HbA1c performed and Morisky Medication Adherence Scale (MMAS-4) questionnaires completed, to assess glycaemic control and compliance with treatment. Results. Of the 379 participants, 61 were known diabetics (16.15%; 95% CI 12.4-19.8%). After exclusion of eight patients with incomplete results, a new diagnosis of DM was made in five out of 310 patients (1.6%; 95% CI 0.2-3.0%). Overall prevalence of DM was 17.8% (66/371; 95% CI 13.9-21.7%). HbA1c results were available in 57 (93.4%) of the 61 known diabetics. Of these 27 (47.4%; 95% CI 34.4-60.3%) had an HbA1c level≥8.5% and 14 (24.6%; 95% CI 13.4 - 35.8%) had an HbA1c ≤7%. Based on positive responses to two or more questions on their MMAS-4 questionnaires, 12 out of 60 participants (20%) were deemed non-compliant. Conclusion. There is a low rate of undiagnosed DM in our elective surgical population; however there is a large proportion of poorly controlled DM. Since poorly controlled DM is known to increase postoperative complications, this likely increases the burden of perioperative care. Resources should be focused on improvement of long-term glycaemic control in patients presenting for elective surgery.

Acetone in exhaled breath is gaining attention as a non-invasive means of quantifying blood glucose levels in Diabetics. This calls for development of novel biosensors for the detection of trace concentrations of acetone present in human breath. Traditional gas detection systems, such as GC/MS and chemiresistive sensors, are currently used for this purpose. However, these systems have limitations with regards to size, cost, and operating temperature. This work presents the K2W7O22/Ti3C2 nanocomposite sensor as breath acetone sensor that overcomes the limitations in traditional detection systems. Sensing experiments were conducted using 5 different sensor materials in varying ratios. KWO/Ti3C2 - ratio 2:1 (annealed) and KWO/Ti3C2 - ratio 2:1 (Unannealed) showed excellent sensitivity to 2.85ppm and 5.4ppm acetone concentration. These materials were then implemented in a prototype device. Material and device test results confirm the potentials of the novel KWO/Ti3C2 nanocomposite as a good sensor for breath acetone detection.

Currently, the etiology of obesity is conceptualized as a confluence of environmental, socioeconomic, behavioral, biological and genetic factors. With regard to behavioral factors, some have suggested that a failure of self-control may contribute to the difficulty of an overweight/obese individual because of their inability to resist food or maintain physical activity. Recent research proposed that self-control could be described as similar to a muscle that can be fatigued. Thus, if an individual engages in a self-control task they have lessened ability to utilize self-control on a subsequent task. Theory also suggests self-control may be fueled by a finite resource, identified as blood glucose. The role blood glucose plays is important to understand, especially in overweight and obese populations, as they may be more likely to be insulin resistant. In effect overweight and obese individuals are less likely to adequately process glucose. Therefore overweight/obese individuals might react to self-control tasks differently than normal weight individuals. Participants who were considered normal weight, overweight, and obese were recruited from the UNT research pool. They answered questions about their trait self-control in daily life and engaged in either a task that required them to exert self-control (e.g., resist crossing out a letter unless criteria is met) or a control task (e.g., cross out a letter without restriction). All participants then engaged in a subsequent self-control task to assess if engaging in the initial self-control task reduced performance on the subsequent self-control task compared to the control task. The current research findings were not in line with previous research, in that a depletion effect in self-control was not observed; in neither the normal weight individuals nor the overweight and obese groups. There were several limitations that may have contributed to these findings including; higher DSC than observed in the general population and a possible adaptation effect due to the duration of the self-control tasks, which is in keeping with subsequently published research.

The glycaemic index (GI) is a measurement used to classify foods according to their potential for raising blood glucose levels. The GI of a foodstuff is generally measured by determining the increment in blood glucose concentration after the consumption of a test meal over a set period of time and comparing it with an isoglucosidic control meal (normally white bread or glucose) and expressed as a percentage within a group of individuals (in vivo). Rapid analysis methods (in vitro) are being developed and evaluated worldwide, and in many cases the values obtained have correlated well with the GI values determined by in vivo methods. The criticism against rapid analysis methods is that the methods do not provide numerical GI values. Proposed labelling legislation in South Africa recommends that suppliers should only indicate if the product has a high, intermediate or low GI. The purpose of this study was to investigate existing rapid assessment methods for the prediction of GI, and develop such a method for South Africa to be used by food producers as a screening tool during product development in line with the newly proposed national labelling requirements. The preliminary studies on the developed rapid assessment method indicated good repeatability (CV 0.78%), reproducibility and precision (CV 3.5%). Further comparative trials indicated that the in vitro method accurately predicts the GI category of Almera potatoes (Solanum Tuberosum L. cultivar Almera) and Gero fat free litchi and raspberry flavoured yoghurt, in line with results found from in vivo analysis. Significant inter-laboratory variability of in vivo analysis of GI values obtained for the Almera potato cultivar was found, and the need for future alignment of methodology and sample preparation is recommended./p> / Dissertation (MSc)--University of Pretoria, 2010. / Food Science / unrestricted

Question: Can passive static stretching lower blood glucose in an at-risk population? Design: Randomised, within-participant experimental study. Participants: 22 adults (17 males) either at increased risk of Type 2 diabetes or with Type 2 diabetes. Intervention: The participants reported to the laboratory 2. hr after eating a meal, and drank 355. ml of fruit juice (∼43. g carbohydrate). Thirty minutes later, they underwent either a 40. min passive static stretching regimen or a mock passive stretching regimen. Stretching consisted of six lower body and four upper body static passive stretches. For the mock stretches, the same positions were adopted, but no tension was applied to the musculature. Outcome measures: Blood glucose levels for both the stretching and mock stretching were analysed from a finger prick sample using a hand-held glucometer. Values were obtained at baseline (0. min), during the regimen (20. min), and after the regimen (40. min) on both study days. Results: Compared to mock stretch, stretching resulted in a significantly greater drop in blood glucose at 20. min (mean difference 28. mg/dL, 95% CI 13 to 43; or 1.57. mmol/L, 95% CI 0.72 to 2.39). This effect was also statistically significant at 40. min (mean difference 24. mg/dL, 95% CI 9 to 39; or 1.35. mmol/L, 95% CI 0.50 to 2.17). Conclusion: These results suggest that passive static stretching of the skeletal muscles may be an alternative to exercise to help lower blood glucose levels.

Doctor Educationis / Diabetes has since been a global epidemic; an estimated 5.0 million deaths of diabetes in the world have been recorded; one in 11 adults have diabetes (415 million); and by 2040, one adult in 10 (642 million) will have diabetes. In Africa, more than two thirds of people with diabetes are undiagnosed, and 42 million have diabetes in the Sub-Saharan region with 324 877 adult deaths in South Africa (IDF, 2015). The global prevalence (age-standardized) of diabetes has nearly doubled since 1980,rising from 4.7% to 8.5% in the adult population. This reflects an increase associated with risk factors such as overweight or obese (WHO, 2016). Medicinal plants on the other hand, have played a significant role in the treatment and prevention of diabetes for centuries. In South Africa, indigenous medicinal plants have increasingly been used in the treatment of diabetes. In this study, a new anti-diabetes herbal compound named Jiang Tang 2016 (JT2016), made of three well researched South African indigenous medicinal plants is investigated for its hypoglycemic effects in HFD/STZ induced diabetic SD rats. These plants have been used for centuries in the indigenous system of medicine against various ailments, they are easily accessible, they grow in abundance, and are economically sustainable. Aim The aim of this study was to investigate the hypoglycemic effects and safety of the anti- diabetes herbal compound, Jiang Tang 2016 (JT2016) in HFD/STZ induced diabetic SD rats

The author deals with oxidative stress and its effects on the pathogenesis of various diseases including the development of insulin resistance. The work is divided in the usual way overview of current knowledge on the issues, methods, results, discussion and conclusions. Part of this work is to describe an animal experiment in the waking state, whose introduction to our department was one of the tasks of this graduate work.

No description available.

Obesity is characterized by hyperinsulinemia and chronic inflammation, contributing to insulin resistance and type 2 diabetes (T2D) risk. Pattern recognition receptors (PRRs) of the innate immune system, including Toll-like Receptors (TLRs) and Nod-like Receptors (NLRs), have been identified as propagators of metabolic inflammation. Circulating bacterial components exert distinct effects on inflammation and insulin sensitivity via TLRs and NLRs. Specific types of bacterial peptidoglycan engage NOD1 and NOD2. Activators of NOD1 increase inflammation and insulin resistance, while activators of NOD2 promote immune tolerance and insulin sensitivity. NOD1 and NOD2 use the common downstream adaptor RIPK2 to drive immune responses, but the role of RIPK2 in glucose homeostasis was unknown. RIPK2 is positioned to mediate effects of xenobiotics and microbial components on blood glucose. For example, tyrosine kinase inhibitors (TKIs) are being investigated for diabetes treatment. Improvements in blood glucose control have been observed in diabetic cancer patients receiving TKI therapy but the mechanism underlying these changes remains unclear. Several TKIs inhibit RIPK2. We sought to understand if TKIs that inhibit RIPK2 block inflammatory and metabolic consequences of NOD signalling. We hypothesized inhibition of inflammation via NOD1-RIPK2 by certain TKIs contributes to lowered blood glucose/improved insulin sensitivity in pre-clinical models of obesity. We showed that RIPK2 was required for acute glycemic consequences of NOD1 and NOD2 activation, and RIPK2-specific TKIs attenuated these glycemic effects. We found TKI-mediated improvements in blood glucose are independent of NOD-RIPK2 signalling during diet-induced obesity. However, RIPK2 mediated the effects of certain TKIs on blood insulin. Finally, we tested if RIPK2 mediated the effects of bacterial components derived from commensal microbiota. We found injection of upper intestinal microbe components lowered blood glucose via NOD2-RIPK2 signalling. These findings demonstrate that modulation of RIPK2 signalling by xenobiotic or microbial factors is an important contributor to blood glucose and insulin homeostasis. / Thesis / Doctor of Philosophy (PhD) / Obesity increases the risk of chronic diseases, including Type 2 Diabetes (T2D). Obesity stops insulin from working properly, leading to the inability to lower blood glucose. Obesity and T2D are linked to chronic, low-grade activation of the immune system. The immune system normally defends the body against microbes by inducing a pro-inflammatory response. Inflammation can also be activated or inhibited by drugs (xenobiotics), and different aspects of inflammation can increase or decrease blood glucose and insulin. A major unanswered question was how certain cancer drugs and bacterial components interact with the immune system to change blood glucose or insulin. This work tested how an innate immune pathway that detects bacterial cell wall components is influenced by cancer drugs and alters blood glucose and insulin in pre-clinical models. This work is targeted at understanding how new prebiotics or existing drugs can be tasked as therapeutic strategies for prediabetes and T2D.