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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin resistance (IR) is a phenomenon which associates several serious "diseases of civilization" within the framework of Reaven's metabolic syndrome. In the submitted paper the authors describe the so-called "paradox of insulin resistance"--a paradoxical finding of inadequate insulin action under laboratory induced conditions while under "common" conditions the finding is reversed. Diabetes mellitus type 2 (with obesity) is characterized by excessive filling of cells by energetically rich substances. A low energy output, inadequate physical activity in these subjects leads to the development of regulatory mechanisms, which restrict further nutrient (glucose) uptake from blood into cells. During subsequent stages of the disease the excessive glucose uptake by adipose tissue cells and muscle is ensured by the high concentration gradient, hyperglycaemia and hyperinsulinaemia. Induction of "comparable" conditions in clamp studies leads to paradoxical results. During relative hypoglycaemia and hypoinsulinaemia (as compared with normal conditions) the tissues of the diabetic patient, due to regulatory mechanisms, take up a smaller amount of glucose than tissues of non-diabetic subjects (although under normal conditions the glucose uptake is higher). This phenomenon is called "Paradox of insulin resistance". In a major proportion of patients IR can be induced by mere maintenance of hyperinsulinaemia, it can be minimalized by reducing the nutrient intake and by increasing physical exertion. Differentiation of patients where IR is a secondary, regulatory phenomenon is one of the basic tasks of the physician. Only patients who suffer from primary disorders of insulin function, primary IR and true insulin deficiency should be treated by administration of hyperinsulinaemia inducing drugs. It is questionable how suitable it is to administer these drugs to patients who suffer from a life-style disorder and are threatened by complications associated with hyperinsulinism.
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PMID:[The paradox of insulin resistance]. 1095 72

Research on the efficacy of hypnosis in the treatment of eating disorders has produced mixed findings. This is due in part to the interplay between the characteristics of people with eating disorders and the phenomena of hypnosis. In addition, several authors have noted that methodological limitations in hypnosis research often make evaluation of treatment efficacy difficult. Many of the studies extant provide insufficient information regarding the specifics of the hypnotic intervention(s) to facilitate replication and clinical implementation. Therefore, this paper only reviews literature with replicable methodological descriptions. It focuses on the three primary disorders of interest to clinicians: bulimia nervosa, anorexia nervosa, and obesity. The implications for evaluating treatment efficacy are discussed.
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PMID:Efficacy of hypnotherapy in the treatment of eating disorders. 1755 21

Insulin resistance is among the most prevalent endocrine derangements in the world, and it is closely associated with major diseases of global reach including diabetes mellitus, atherosclerosis, nonalcoholic fatty liver disease, and ovulatory dysfunction. It is most commonly found in those with obesity but may also occur in an unusually severe form in rare patients with monogenic defects. Such patients may loosely be grouped into those with primary disorders of insulin signaling and those with defects in adipose tissue development or function (lipodystrophy). The severe insulin resistance of both subgroups puts patients at risk of accelerated complications and poses severe challenges in clinical management. However, the clinical disorders produced by different genetic defects are often biochemically and clinically distinct and are associated with distinct risks of complications. This means that optimal management of affected patients should take into account the specific natural history of each condition. In clinical practice, they are often underdiagnosed, however, with low rates of identification of the underlying genetic defect, a problem compounded by confusing and overlapping nomenclature and classification. We now review recent developments in understanding of genetic forms of severe insulin resistance and/or lipodystrophy and suggest a revised classification based on growing knowledge of the underlying pathophysiology.
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PMID:Genetic syndromes of severe insulin resistance. 2153 11

Hormones produced by the adrenal glands and adipose tissues have important roles in normal physiology and are altered in many disease states. Obesity is associated with changes in adrenal function, including increase in adrenal medullary catecholamine output, alterations of the hypothalamic-pituitary-adrenal (HPA) axis, elevations in circulating aldosterone together with changes in adipose tissue glucocorticoid metabolism, and enhanced adipocyte mineralocorticoid receptor activity. It is unknown whether these changes in adrenal endocrine function are in part responsible for the pathogenesis of obesity and related comorbidities or represent an adaptive response. In turn, adipose tissue hormones or "adipokines" have direct effects on the adrenal glands and interact with adrenal hormones at several levels. Here we review the emerging evidence supporting the existence of "cross talk" between the adrenal gland and adipose tissue, focusing on the relevance and roles of their respective hormones in health and disease states including obesity, metabolic syndrome, and primary disorders of the adrenals.
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PMID:Adipose tissue and adrenal glands: novel pathophysiological mechanisms and clinical applications. 2501 68

Insulin orchestrates physiological responses to ingested nutrients; however, although it elicits widely ramifying metabolic and trophic responses from diverse tissues, 'insulin resistance (IR)', a pandemic metabolic derangement commonly associated with obesity, is usually defined solely by blunting of insulin's hypoglycaemic effect. Recent study of monogenic forms of IR has established that biochemical subphenotypes of IR exist, clustering into those caused by primary disorders of adipose tissue and those caused by primary defects in proximal insulin signalling. IR is often first recognised by virtue of its associated disorders including type 2 diabetes, dyslipidaemia (DL), fatty liver and polycystic ovary syndrome (PCOS). Although these clinically observed associations are confirmed by cross-sectional and longitudinal population-based studies, causal relationships among these phenomena have been more difficult to establish. Single gene IR is important to recognise in order to optimise clinical management and also permits testing of causal relationships among components of the IR syndrome using the principle of Mendelian randomisation. Thus, where a precisely defined genetic defect is identified that directly produces one component of the syndrome, then phenomena that are causally linked to that component should be seen. Where this is not the case, then a simple causal link is refuted. This article summarises known forms of monogenic severe IR and considers the lessons to be learned about the pathogenic mechanisms both upstream from common IR and those downstream linking it to disorders such as DL, fatty liver, PCOS and cancer.
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PMID:EJE PRIZE 2015: How does insulin resistance arise, and how does it cause disease? Human genetic lessons. 2686 83