The Experts below are selected from a list of 15219 Experts worldwide ranked by ideXlab platform
Michael J Quon - One of the best experts on this subject based on the ideXlab platform.
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current approaches for assessing insulin sensitivity and resistance in vivo advantages limitations and appropriate usage
American Journal of Physiology-endocrinology and Metabolism, 2008Co-Authors: Ranganath Muniyappa, Hui Chen, Michael J QuonAbstract:Insulin resistance contributes to the Pathophysiology of Diabetes and is a hallmark of obesity, metabolic syndrome, and many cardiovascular diseases. Therefore, quantifying insulin sensitivity/resi...
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current approaches for assessing insulin sensitivity and resistance in vivo advantages limitations and appropriate usage
American Journal of Physiology-endocrinology and Metabolism, 2008Co-Authors: Ranganath Muniyappa, Hui Chen, Michael J QuonAbstract:Insulin resistance contributes to the Pathophysiology of Diabetes and is a hallmark of obesity, metabolic syndrome, and many cardiovascular diseases. Therefore, quantifying insulin sensitivity/resistance in humans and animal models is of great importance for epidemiological studies, clinical and basic science investigations, and eventual use in clinical practice. Direct and indirect methods of varying complexity are currently employed for these purposes. Some methods rely on steady-state analysis of glucose and insulin, whereas others rely on dynamic testing. Each of these methods has distinct advantages and limitations. Thus, optimal choice and employment of a specific method depends on the nature of the studies being performed. Established direct methods for measuring insulin sensitivity in vivo are relatively complex. The hyperinsulinemic euglycemic glucose clamp and the insulin suppression test directly assess insulin-mediated glucose utilization under steady-state conditions that are both labor and time intensive. A slightly less complex indirect method relies on minimal model analysis of a frequently sampled intravenous glucose tolerance test. Finally, simple surrogate indexes for insulin sensitivity/resistance are available (e.g., QUICKI, HOMA, 1/insulin, Matusda index) that are derived from blood insulin and glucose concentrations under fasting conditions (steady state) or after an oral glucose load (dynamic). In particular, the quantitative insulin sensitivity check index (QUICKI) has been validated extensively against the reference standard glucose clamp method. QUICKI is a simple, robust, accurate, reproducible method that appropriately predicts changes in insulin sensitivity after therapeutic interventions as well as the onset of Diabetes. In this Frontiers article, we highlight merits, limitations, and appropriate use of current in vivo measures of insulin sensitivity/resistance.
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quantitative insulin sensitivity check index a simple accurate method for assessing insulin sensitivity in humans
The Journal of Clinical Endocrinology and Metabolism, 2000Co-Authors: Arie Katz, Sridhar S Nambi, Kieren J Mather, Alain D Baron, Dean Follmann, Gail Sullivan, Michael J QuonAbstract:Insulin resistance plays an important role in the Pathophysiology of Diabetes and is associated with obesity and other cardiovascular risk factors. The “gold standard” glucose clamp and minimal model analysis are two established methods for determining insulin sensitivity in vivo, but neither is easily implemented in large studies. Thus, it is of interest to develop a simple, accurate method for assessing insulin sensitivity that is useful for clinical investigations. We performed both hyperinsulinemic isoglycemic glucose clamp and insulin-modified frequently sampled iv glucose tolerance tests on 28 non-obese, 13 obese, and 15 type 2 diabetic subjects. We obtained correlations between indexes of insulin sensitivity from glucose clamp studies (SIClamp) and minimal model analysis (SIMM) that were comparable to previous reports (r = 0.57). We performed a sensitivity analysis on our data and discovered that physiological steady state values [i.e. fasting insulin (I0) and glucose (G0)] contain critical informa...
Ranganath Muniyappa - One of the best experts on this subject based on the ideXlab platform.
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current approaches for assessing insulin sensitivity and resistance in vivo advantages limitations and appropriate usage
American Journal of Physiology-endocrinology and Metabolism, 2008Co-Authors: Ranganath Muniyappa, Hui Chen, Michael J QuonAbstract:Insulin resistance contributes to the Pathophysiology of Diabetes and is a hallmark of obesity, metabolic syndrome, and many cardiovascular diseases. Therefore, quantifying insulin sensitivity/resi...
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current approaches for assessing insulin sensitivity and resistance in vivo advantages limitations and appropriate usage
American Journal of Physiology-endocrinology and Metabolism, 2008Co-Authors: Ranganath Muniyappa, Hui Chen, Michael J QuonAbstract:Insulin resistance contributes to the Pathophysiology of Diabetes and is a hallmark of obesity, metabolic syndrome, and many cardiovascular diseases. Therefore, quantifying insulin sensitivity/resistance in humans and animal models is of great importance for epidemiological studies, clinical and basic science investigations, and eventual use in clinical practice. Direct and indirect methods of varying complexity are currently employed for these purposes. Some methods rely on steady-state analysis of glucose and insulin, whereas others rely on dynamic testing. Each of these methods has distinct advantages and limitations. Thus, optimal choice and employment of a specific method depends on the nature of the studies being performed. Established direct methods for measuring insulin sensitivity in vivo are relatively complex. The hyperinsulinemic euglycemic glucose clamp and the insulin suppression test directly assess insulin-mediated glucose utilization under steady-state conditions that are both labor and time intensive. A slightly less complex indirect method relies on minimal model analysis of a frequently sampled intravenous glucose tolerance test. Finally, simple surrogate indexes for insulin sensitivity/resistance are available (e.g., QUICKI, HOMA, 1/insulin, Matusda index) that are derived from blood insulin and glucose concentrations under fasting conditions (steady state) or after an oral glucose load (dynamic). In particular, the quantitative insulin sensitivity check index (QUICKI) has been validated extensively against the reference standard glucose clamp method. QUICKI is a simple, robust, accurate, reproducible method that appropriately predicts changes in insulin sensitivity after therapeutic interventions as well as the onset of Diabetes. In this Frontiers article, we highlight merits, limitations, and appropriate use of current in vivo measures of insulin sensitivity/resistance.
Kenichi Nibu - One of the best experts on this subject based on the ideXlab platform.
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increased inner ear susceptibility to noise injury in mice with streptozotocin induced Diabetes
Diabetes, 2012Co-Authors: Takeshi Fujita, Daisuke Yamashita, Sayaka Katsunuma, Shingo Hasegawa, Hitoshi Tanimoto, Kenichi NibuAbstract:We aimed to investigate the Pathophysiology of Diabetes-associated hearing impairment in type 1 Diabetes using mice with streptozotocin-induced Diabetes (C57BL/6J; male). Hearing function was evaluated 1, 3, and 5 months after induction of Diabetes (five diabetic and five control animals per time point) using auditory-evoked brain stem responses (ABRs). Mice (four diabetic and four control) were exposed to loud noise (105 dB) 5 months after induction of Diabetes. ABRs were measured before and after noise exposure. Cochlear blood flows were measured by laser-Doppler flowmeter. Spiral ganglion cells (SGCs) were counted. Vessel endothelial cells were observed by CD31 immunostaining. Chronologic changes in the ABR threshold shift were not significantly different between the diabetic and control groups. However, vessel walls in the modiolus of the cochleae were significantly thicker in the diabetic group than the control group. Additionally, recovery from noise-induced injury was significantly impaired in diabetic mice. Reduced cochlea blood flows and SGC loss were observed in diabetic mice cochleae after noise exposure. Our data suggest that diabetic cochleae are more susceptible than controls to loud noise exposure, and decreased cochlear blood flow due to sclerosis of the vessels and consequent loss of SGCs are possible mechanisms of hearing impairment in diabetic patients.
Ronald C Kahn - One of the best experts on this subject based on the ideXlab platform.
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cross talk between insulin and wnt signaling in preadipocytes role of wnt co receptor low density lipoprotein receptor related protein 5 lrp5
Journal of Biological Chemistry, 2012Co-Authors: Jane Palsgaard, Brice Emanuelli, Jonathon N Winnay, Grzegorz Sumara, Gerard Karsenty, Ronald C KahnAbstract:Disturbed Wnt signaling has been implicated in numerous diseases, including type 2 Diabetes and the metabolic syndrome. In the present study, we have investigated cross-talk between insulin and Wnt signaling pathways using preadipocytes with and without knockdown of the Wnt co-receptors LRP5 and LRP6 and with and without knock-out of insulin and IGF-1 receptors. We find that Wnt stimulation leads to phosphorylation of insulin signaling key mediators, including Akt, GSK3β, and ERK1/2, although with a lower fold stimulation and slower time course than observed for insulin. These Wnt effects are insulin/IGF-1 receptor-dependent and are lost in insulin/IGF-1 receptor double knock-out cells. Conversely, in LRP5 knockdown preadipocytes, insulin-induced phosphorylation of IRS1, Akt, GSK3β, and ERK1/2 is highly reduced. This effect is specific to insulin, as compared with IGF-1, stimulation and appears to be due to an inducible interaction between LRP5 and the insulin receptor as demonstrated by co-immunoprecipitation. These data demonstrate that Wnt and insulin signaling pathways exhibit cross-talk at multiple levels. Wnt induces phosphorylation of Akt, ERK1/2, and GSK3β, and this is dependent on insulin/IGF-1 receptors. Insulin signaling also involves the Wnt co-receptor LRP5, which has a positive effect on insulin signaling. Thus, altered Wnt and LRP5 activity can serve as modifiers of insulin action and insulin resistance in the Pathophysiology of Diabetes and metabolic syndrome.
Yong Li - One of the best experts on this subject based on the ideXlab platform.
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MicroRNAs: a new ray of hope for Diabetes mellitus
Protein & Cell, 2012Co-Authors: Munish Kumar, Sayantan Nath, Himanshu K. Prasad, G. D. Sharma, Yong LiAbstract:Diabetes mellitus has become one of the most common chronic diseases, thereby posing a major challenge to global health. Characterized by high levels of blood glucose (hyperglycemia), Diabetes usually results from a loss of insulin-producing β-cells in the pancreas, leading to a deficiency of insulin (type 1 Diabetes), or loss of insulin sensitivity (type 2 Diabetes). Both types of Diabetes have serious secondary complications, such as microvascular abnormalities, cardiovascular dysfunction, and kidney failure. Various complex factors, such as genetic and environmental factors, are associated with the Pathophysiology of Diabetes. Over the past two decades, the role of small, single-stranded noncoding microRNAs in various metabolic disorders, especially Diabetes mellitus and its complications, has gained widespread attention in the scientific community. Discovered first as an endogenous regulator of development in the nematode Caenorhabditis elegans , these small RNAs post-transcriptionally suppress mRNA target expression. In this review, we discuss the potential roles of different microRNAs in Diabetes and Diabetes-related complications.