Insulin resistance and metabolic profile in antipsychotic naïve schizophrenia patients

Dasgupta, Anindya; Singh, Om Prakash; Rout, Jayanta Kumar; Saha, Tanmay; Mandal, Sonai

doi:10.1016/j.pnpbp.2010.06.011

Cited by 52 publications

(55 citation statements)

References 42 publications

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“…Olanzapine, which antagonizes serotonin more than dopamine, histamine, or GABA receptors, results in a weight gain of approximately 2 lb (0.9 kg) per month in humans [112]. Considerable evidence shows olanzapine acutely increases fat accumulation [113][114][115][116]. There is also evidence that polymorphisms in the serotonin receptor are associated with metabolic syndrome in patients on olanzapine or clozapine, another serotonin antagonist [117,118].…”

Section: Neurotransmittersmentioning

confidence: 99%

Hypothalamic control of energy and glucose metabolism

Sisley

Sandoval

2011

Rev Endocr Metab Disord

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The central nervous system (CNS), generally accepted to regulate energy homeostasis, has been implicated in the metabolic perturbations that either cause or are associated with obesity. Normally, the CNS receives hormonal, metabolic, and neuronal input to assure adequate energy levels and maintain stable energy homeostasis. Recent evidence also supports that the CNS uses these same inputs to regulate glucose homeostasis and this aspect of CNS regulation also becomes impaired in the face of dietary-induced obesity. This review focuses on the literature surrounding hypothalamic regulation of energy and glucose homeostasis and discusses how dysregulation of this system may contribute to obesity and T2DM.

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Section: Neurotransmittersmentioning

confidence: 99%

Hypothalamic control of energy and glucose metabolism

Sisley

Sandoval

2011

Rev Endocr Metab Disord

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“…There is a body of evidence to suggest that schizophrenia itself may be linked to an increased risk of glucose dysregulation, although the data remain contradictory on this point. [46][47][48][49][50] More consistent are the findings that, at least prior to the onset of FEP, schizophrenia is not associated with increased risk of obesity. [48][49][50][51][52][53] Indeed, several reports have suggested that an FEP is associated with lower BMI values than seen in control subjects.…”

Section: The Association Between Schizophrenia and Obesitymentioning

confidence: 54%

Beyond Pharmacotherapy: Understanding the Links between Obesity and Chronic Mental Illness

et al. 2012

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While differences in weight-gain potential exist, both between and within classes of psychiatry medications, most commonly used atypical antipsychotics, mood stabilizers, and antidepressants result in some degree of weight gain. This is not new information and it requires an understanding of the tolerability profiles of different treatments and their goodness of fit with specific patient phenotypes. However, this iatrogenic association represents only a piece of this obesity-mental illness dyad. The complex interplay between psychiatric illness and weight involves neurobiology, psychology, and sociological factors. Parsing the salient variables in people with mental illness is an urgent need insofar as mortality from physical health causes is the most common cause of premature mortality in people with chronic mental illness. Our review examines issues associated with common chronic mental illnesses that may underlie this association and warrant further study if we hope to clinically intervene to control this life-threatening comorbidity. W W WBien que les différences de potentiel de gain de poids existent, à la fois entre les classes de médicaments psychiatriques et au sein de celles-ci, les antipsychotiques atypiques, les psychorégulateurs et les antidépresseurs les plus fréquemment utilisés entraînent à un certain degré une prise de poids. Cette information n'a rien de neuf et elle demande une compréhension des profils de tolérabilité de différents traitements et de leur qualité d'ajustement aux phénotypes spécifiques du patient. Cependant, cette association iatrogène ne représente qu'une pièce de ce tandem obésité-maladie mentale. L'action réciproque complexe entre la maladie psychiatrique et le poids met en jeu la neurobiologie, la psychologie et les facteurs sociologiques. L'analyse des variables prépondérantes chez les personnes souffrant de maladie mentale est un besoin urgent pour autant que la mortalité attribuable à des causes de santé physique est la cause la plus commune de mortalité prématurée chez les personnes souffrant de maladie mentale chronique. Notre étude examine les questions associées aux maladies mentales chroniques communes qui peuvent sous-tendre cette association et justifient plus de recherche si nous souhaitons intervenir cliniquement pour contrôler cette comorbidité qui met la vie en danger.

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“…As a widely validated clinical and epidemiological tool for estimating insulin resistance and β cell function, the homeostasis model assessment (HOMA) is derived from a mathematical assessment of the balance between hepatic glucose output and insulin secretion from fasting levels of glucose and insulin (14,21,22) . This model requires only single measurement of insulin and glucose in the basal state and so, in some conditions, is a suitable alternative for large-scale epidemiologic studies to the sophisticated "gold standard" methods which usually require dynamic data via costly and invasive procedures.…”

Section: Computation Of Insulin Resistance (21-23)mentioning

confidence: 99%

“…This model requires only single measurement of insulin and glucose in the basal state and so, in some conditions, is a suitable alternative for large-scale epidemiologic studies to the sophisticated "gold standard" methods which usually require dynamic data via costly and invasive procedures. HOMA IR is computed with the formula: fasting plasma glucose (mmol/l) times fasting serum insulin (mIU/l) divided by 22.5 (14,23) .…”

Section: Computation Of Insulin Resistance (21-23)mentioning

confidence: 99%

“…Uzar et al (2012) stated that there is increased plasma prolidase enzyme activity in neuropathy due to diabetes (DN) as evidence of increased collagen turnover (10) . Homeostatic model assessment-insulin resistance (HOMA IR) reflects insulin resistance and is associated with increased prevalence of impaired glucose tolerance (IGT) and type 2 diabetes in several populations (11)(12)(13)(14) . We found insufficient and conflicting data regarding plasma prolidase activity, oxidative stress and their role in development of microvascular complications like neuropathy in patients with diabetes.…”

Section: Introductionmentioning

confidence: 99%

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Variation of Prolidase Activity: A Predictor of Neuropathy due to Diabetes Mellitus?

Rout¹

2017

jmscr

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Prolidase is a member of the matrix metalloproteinase family responsible for collagen turnover which is implicated in the pathogenesis of diabetic neuropathy (DN). 50 (F-16, M-34) subjects suffering from T2DM, 46 subjects (F-21, M-25) with Myara et al. (1984) p<0.001) and prolidase (t=5.968, p<0.001) were significantly higher in group 2 than in group 1. These findings imply a strong association between insulin resistance and increased collagen turnover in T2DM. ANOVA was performed and a strong statistical association was found in case of p<0.001)

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Insulin resistance and metabolic profile in antipsychotic naïve schizophrenia patients

Cited by 52 publications

References 42 publications

Hypothalamic control of energy and glucose metabolism

Hypothalamic control of energy and glucose metabolism

Beyond Pharmacotherapy: Understanding the Links between Obesity and Chronic Mental Illness

Variation of Prolidase Activity: A Predictor of Neuropathy due to Diabetes Mellitus?

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