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Weight Concerns
Published in Carolyn Torkelson, Catherine Marienau, Beyond Menopause, 2023
Carolyn Torkelson, Catherine Marienau
The term insulin resistance (also called insulin sensitivity) means that insulin, which is produced by the pancreas, can’t transport glucose from the bloodstream into the body’s cells. When insulin doesn’t open the cell door to let glucose in, the cell is starved of glucose and sends the brain a signal that it is hungry. The glucose left sitting outside the cells increases the blood sugar level, which can lead to type 2 diabetes, and the extra glucose is stored as fat, which can lead to central obesity.
Brain Insulin Action in the Control of Metabolism in Humans
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
The mixture of different nutrients in a meal triggers several physiological reactions in the periphery and the CNS. Hence, a more standardized way to study insulin action is the oral glucose tolerance test (oGTT), which is strongly implemented in the clinical routine. After oral ingestion of a 75 g glucose solution, blood glucose rises and several endocrine factors, including insulin, are released into the circulation. Peripheral insulin sensitivity can be assessed from this test e.g. by the oGTT-derived Matsuda insulin sensitivity index (39) and insulin secretion can be estimated e.g. by the oral Disposition Index (40). Insulin secretion can also be stimulated by an iv glucose bolus during an iv glucose tolerance test (ivGTT) (41) or by hyperglycemic glucose clamps (42). While the intravenous route of glucose administration is not physiological, it has the advantage of stimulating insulin release without major effects on several other endocrine systems that are activated after oral food or glucose intake, such as incretins, which also act in the brain (43). For both tests, several indices are available to assess peripheral insulin sensitivity and insulin secretion.
Diabetes, Overweight, and Obesity
Published in Michelle Tollefson, Nancy Eriksen, Neha Pathak, Improving Women's Health Across the Lifespan, 2021
Women with a low-risk lifestyle (no smoking, ≥150 min/wk of moderate to vigorous physical activity, healthy diet, and body mass index [BMI] <25 before pregnancy) had a 52% lower risk of GDM compared to all other pregnancies.30 Improving insulin sensitivity with a healthy diet, physical activity, and metformin may reduce the risk of diabetes in women with insulin resistance.24
Effect of a single bout of resistance exercise on zinc-α2-glycoprotein
Published in Archives of Physiology and Biochemistry, 2022
Michihiro Kon, Yasuhiro Suzuki
Insulin resistance is a main contributor to metabolic diseases, such as cardiovascular disease and type 2 diabetes mellitus. Regular physical exercise training, in particular aerobic exercise training, has been conventionally recommended as a therapeutic and effective training regimen for metabolic diseases because it improves metabolism and insulin sensitivity (Hawley 2004). In contrast, recently, it has been reported that resistance exercise training, which causes muscle hypertrophy and improvement in muscle function, also leads to favourable metabolic adaptations in skeletal muscle (Kim et al. 2015) and the whole body (Umpierre et al. 2011). Kim et al. (2015) demonstrated that an increase in expression and translocation of glucose transporter 4 (GLUT4), which is related to glucose uptake in skeletal muscle, was induced within 8 weeks of resistance training. In addition, a recent systematic review by Umpierre et al. (2011) showed that resistance training improved insulin resistance. Based on these results, resistance training as well as aerobic training may be an effective training method that improves insulin sensitivity. However, the mechanisms of resistance training-induced improvements in energy metabolism and insulin sensitivity have not been fully understood.
Safety of current recombinant human growth hormone treatments for adults with growth hormone deficiency and unmet needs
Published in Expert Opinion on Drug Safety, 2020
Charlotte Höybye, Paolo Beck-Peccoz, Suat Simsek, Markus Zabransky, Hichem Zouater, Günter Stalla, Robert D Murray
Over time several studies have documented that most of the symptoms and signs of the adult GHD syndrome are improved or reversed by GH replacement therapy (Figure 2). In all ages, it increases energy, motivation, self-esteem, social function, and general well-being [19,20]. Short- and long-term studies consistently demonstrate improvement in body composition [6,7,17,20–26] characterized by a reduction in body fat and an increase in muscle mass, including an increase in muscle strength and physical capacity [27]. Cardiovascular risk factors and cardiac function are improved [28]. Circulating markers for bone formation and bone reabsorption increase, however, improvement in bone mineral density is delayed but maintained during long-term treatment [20,23,29,30]. A dual effect on insulin sensitivity has been reported; in some patients insulin sensitivity is impaired while in others improved [29]. Most likely, the improvement is caused by the simultaneous improvement in body composition and physical activity, while the impairment could be a result of the physiological effects of GH on glucose metabolism. During GH treatment beneficial effects on circulating lipids have been shown, e.g. a decrease in total and LDL cholesterol [6,7,17,20–26,29]. An improvement in blood lipids and other cardiovascular risk markers are documented to be maintained even after 15 years of GH treatment [26].
Effects of Consuming Almonds on Insulin Sensitivity and Other Cardiometabolic Health Markers in Adults With Prediabetes
Published in Journal of the American College of Nutrition, 2020
Orsolya M. Palacios, Kevin C. Maki, Di Xiao, Meredith L. Wilcox, Mary R. Dicklin, Melvyn Kramer, Rupal Trivedi, Britt Burton-Freeman, Indika Edirisinghe
Prediabetes is a primary risk factor for developing type 2 diabetes (T2D) (1), which is a major risk factor for cardiovascular disease (CVD) (2,3). Insulin resistance and pancreatic beta-cell dysfunction are core mediators of T2D development (4); therefore, preserving pancreatic beta-cell function is critical to preventing T2D (5). Increasing insulin sensitivity reduces insulin secretion, which, in turn, reduces beta-cell workload, contributing to the prevention or delay of pancreatic beta-cell dysfunction (5). Lifestyle interventions (e.g., increased physical activity, loss of excess body weight, Mediterranean-style diet intake) that enhance tissue responsiveness to insulin are associated with a lower risk of T2D and improved levels of markers of glucose homeostasis (6–9). In contrast, a diet high in refined starches and added sugars appears to exacerbate disturbances in carbohydrate (CHO) metabolism (10–12).