Topic
Insulin
About: Insulin is a research topic. Over the lifetime, 124295 publications have been published within this topic receiving 5129734 citations. The topic is also known as: human insulin.
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TL;DR: In this paper, the authors dissected mechanisms whereby insulin activates eNOS by using the fluorescent dye DAF-2 to directly measure NO production in single cells and concluded that insulin regulates ENOS activity using a Ca(2+)-independent mechanism requiring phosphorylation of eNos by Akt.
533 citations
TL;DR: A PIR self-report survey was developed and distributed to a large multicity sample of patients with type 2 diabetes who were not taking insulin to examine their willingness to take insulin if it was prescribed and to identify perceived attitudinal barriers to insulin therapy.
Abstract: To achieve tight glycemic control in type 2 diabetic patients, it may be advantageous to introduce insulin therapy much earlier in the disease course (1). Unfortunately, many patients are reluctant to begin insulin and may delay starting insulin therapy for significant periods of time (2,3). Recent evidence suggests that more than one-quarter of patients may refuse insulin therapy once it is prescribed (4). Little is actually known about this phenomenon, often termed “psychological insulin resistance” (PIR), how common it may be, or why patients feel this way. Therefore, we developed and distributed a PIR self-report survey to a large multicity sample of patients with type 2 diabetes who were not taking insulin. The survey examined their willingness to take insulin if it was prescribed and to identify perceived attitudinal barriers to insulin therapy.
Participants at several 1-day conferences for people with diabetes (Taking Control of Your Diabetes) conducted in San Diego, California; Raleigh, North Carolina; Portland, Oregon; Minneapolis, Minnesota; Philadelphia, Pennsylvania; and Honolulu and Hilo, Hawaii completed an anonymous one-page survey concerning insulin attitudes. At the beginning of each conference, an announcement to all participants explained the study, directed them to the questionnaire in their conference syllabus, and asked them to return completed surveys before the conference’s conclusion. The study was approved by the Committee on Human Research at the University of California, San Francisco.
An initial questionnaire item assessed willingness to begin insulin therapy, rated from very willing to not unwilling. Patients also rated on a six-point …
533 citations
TL;DR: This review summarizes the cellular and molecular defects that contribute to the development of insulin resistance in skeletal muscle and reports a mitochondrial defect in oxidative phosphorylation in skeletal Muscle in variety of insulin resistant states.
Abstract: Insulin resistance in skeletal muscle is manifested by decreased insulin-stimulated glucose uptake and results from impaired insulin signaling and multiple post-receptor intracellular defects including impaired glucose transport, glucose phosphorylation, and reduced glucose oxidation and glycogen synthesis. Insulin resistance is a core defect in type 2 diabetes, it is also associated with obesity and the metabolic syndrome. Dysregulation of fatty acid metabolism plays a pivotal role in the pathogenesis of insulin resistance in skeletal muscle. Recent studies have reported a mitochondrial defect in oxidative phosphorylation in skeletal muscle in variety of insulin resistant states. In this review, we summarize the cellular and molecular defects that contribute to the development of insulin resistance in skeletal muscle.
532 citations
TL;DR: The results of this population-based study indicate that adiposity is strongly associated with CRP in healthy, middle-aged women and whether losing weight ameliorates the inflammatory state.
Abstract: —Obesity, the insulin resistance syndrome, and atherosclerosis are closely linked and may all be determinants of an increased acute-phase response. In this study, we examined the relationship of C-reactive protein (CRP) with measures of obesity, variables of the insulin resistance syndrome, and intima-media thickness of the common carotid arteries in 186 healthy, middle-aged women selected from the general population. Associations were assessed by regression analysis. CRP was strongly associated with body mass index (BMI) and waist circumference. CRP was also associated with other variables of the insulin resistance syndrome, including blood pressure, insulin, high density lipoprotein cholesterol, triglycerides, apolipoprotein A1 (inversely), plasminogen activator inhibitor-1 antigen, and tissue-type plasminogen activator antigen. Associations between CRP and the variables of the insulin resistance syndrome disappeared after controlling for BMI but remained significant for plasminogen activator inhibitor-1 antigen only. The association of CRP with common carotid artery intima-media thickness was weak and limited to ever-smokers. BMI explained 29.7% of the variance of CRP, whereas common carotid artery intima-media thickness explained only 3.7%. The results of this population-based study indicate that adiposity is strongly associated with CRP in healthy, middle-aged women. In this population, BMI accounted for the relationship between CRP and other variables of the insulin resistance syndrome. Further studies should determine whether losing weight ameliorates the inflammatory state.
532 citations
TL;DR: Greater insulin resistance was associated with an AD-like pattern of reduced CMRglu in frontal, parietotemporal, and cingulate regions in adults with PD/T2D.
Abstract: Background—Insulin resistance is a causal factor in pre-diabetes and type 2 diabetes (T2D), and also increases the risk of developing Alzheimer’s disease (AD). Reductions in cerebral glucose metabolic rate (CMRglu) as measured by fluorodeoxyglucose positron emission tomography (FDG PET) in parietotemporal, frontal, and cingulate cortex are also associated with increased AD risk, and can be observed years before dementia onset. Objectives—We examined whether greater insulin resistance as indexed by the homeostasis model assessment (HOMA-IR) would be associated with reduced resting CMRglu in areas known to be vulnerable in AD in a sample of cognitively normal adults with newly diagnosed prediabetes or T2D (P-D/T2D). We also determined whether P-D/T2D adults have abnormal patterns of CMRglu during a memory encoding task. Design—Randomized crossover design of resting and activation [F-18] FDG-PET. Setting—University Imaging Center and VA Clinical Research Unit. Participants—Participants included 23 older adults (mean age±SEM=74.4±1.4) with no prior diagnosis of or treatment for diabetes, but who met American Diabetes Association glycemic criteria for pre-diabetes (n=11) or diabetes (n=12) based on fasting or 2-h oral glucose tolerance test (OGTT) glucose values, and 6 adults (mean age±SEM=74.3±2.8) with normal fasting glucose and glucose tolerance. No participant met Petersen criteria for mild cognitive impairment (MCI). Intervention—Fasting participants rested with eyes open in a dimly lit room and underwent resting and cognitive activation [F-18]FDG PET imaging on separate days, in randomized order, at 9 am. Following a 30-min transmission scan, subjects received an intravenous injection of 5 mCi [F-18]FDG, and the emission scan commenced 40 min post-injection. In the activation condition, a 35-min memory encoding task was initiated at the time of tracer injection. Subjects
532 citations