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lipodystrophy/چاقی

پیوند در کلیپ بورد ذخیره می شود
صفحه 1 از جانب 439 نتایج

Immunogenicity associated with metreleptin treatment in patients with obesity or lipodystrophy.

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Recombinant human leptin (metreleptin) improves glycaemia and hypertriglyceridaemia in patients with generalized lipodystrophy; antibody development with in vitro neutralizing activity has been reported. We aimed to characterize antimetreleptin antibody development, including in vitro neutralizing

Prevalence of obesity and its relationship to clinical lipodystrophy in HIV-infected adults on anti-retroviral therapy.

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BACKGROUND Combination antiretroviral therapy (cART) is associated with lipodystrophy (lipoatrophy and lipoaccumulation) and several metabolic abnormalities that together can contribute to an increased cardiovascular risk. The aim of this study was to evaluate the prevalence of obesity in patients

A search for candidate genes for lipodystrophy, obesity and diabetes via gene expression analysis of A-ZIP/F-1 mice.

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Genome scans for diabetes have identified many regions of the human genome that correlate with the disease state. To identify candidate genes for type 2 diabetes, we examined the transgenic A-ZIP/F-1 mouse. This mouse model has no white fat, resulting in abnormal levels of glucose, insulin, and

Lipodystrophy in HIV 1-infected patients: lessons for obesity research.

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Lipodystrophy is a common alteration in HIV 1-infected patients under anti-retroviral treatment. This syndrome is usually associated with peripheral lipoatrophy, central adiposity and, in some cases, lipomatosis, as well as systemic insulin resistance and hyperlipidemia. Research on the

Lipodystrophy and obesity are associated with decreased number of T cells with regulatory function and pro-inflammatory macrophage phenotype.

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In lipodystrophy (LD) adipose tissue function to store lipids is impaired, leading to metabolic syndrome, similar to that found in obesity. Emerging evidence links dysmetabolism with disorders of the immune system. Our aim is to investigate whether T-cell populations with regulatory function and

[Significant two-weeks clinical efficacy of an association between Massaciuccoli peat and sodium chloride water of Undulna Thermae measured on gynoid lipodystrophy in a group of overweight female].

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BACKGROUND Peloid has been popularly used as an effective base in cosmetic preparations, although its biologically-active materials and mechanisms on skin have not yet been fully determined. An association between Massaciuccoli peat and sodium chloride water of Undulna Thermae was evaluated as a

Characterisation of non-obese diabetic patients with marked insulin resistance identifies a novel familial partial lipodystrophy-associated PPARγ mutation (Y151C).

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OBJECTIVE Familial partial lipodystrophy (FPLD) is a rare metabolic disorder with clinical features that may not be readily recognised. As FPLD patients require a specific therapeutic approach, early identification is warranted. In the present study we aimed to identify cases of FPLD among non-obese

Obesity and lipodystrophy--where do the circles intersect?

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Adipose tissue is unique in that it can undergo significant hypertrophy and atrophy, resulting in wide ranges of obesities and lipodystrophies. At the base of this elasticity is the lipid-filled adipocyte, which can either overfill by storing large amounts of triglycerides or shrink to a tiny cell

Eating behaviour in contrasting adiposity phenotypes: Monogenic obesity and congenital generalized lipodystrophy

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Most known types of nonsyndromic monogenic obesity are caused by rare mutations in genes of the leptin-melanocortin pathway controlling appetite and adiposity. In contrast, congenital generalized lipodystrophy represents the most extreme form of leanness in humans caused by recessive mutations in

Lipin, a lipodystrophy and obesity gene.

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Lipodystrophy and obesity represent extreme and opposite ends of the adiposity spectrum and have typically been attributed to alterations in the expression or function of distinct sets of genes. We previously demonstrated that lipin deficiency impairs adipocyte differentiation and causes

Human subcutaneous adipose tissue LPIN1 expression in obesity, type 2 diabetes mellitus, and human immunodeficiency virus--associated lipodystrophy syndrome.

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The aim of this study was to analyze LPIN1 adipose tissue gene expression levels in 3 clinical insulin-resistant conditions-obesity, type 2 diabetes mellitus, and human immunodeficiency virus (HIV)-associated lipodystrophy-and its relationship with adipogenic and inflammatory markers. Subcutaneous

Adipose tissue dysfunction in obesity and lipodystrophy.

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The primary function of adipose tissue is to store energy in the form of triglycerides during periods of energy excess and to release the energy during fasting or starvation as free fatty acids and glycerol. Adipose tissue secretes a variety of peptides called adipocytokines (eg, leptin,

Lipid regulation in lipodystrophy versus the obesity-associated metabolic syndrome: the dissociation of HDL-C and triglycerides.

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BACKGROUND There is an inverse relationship between triglycerides and high-density lipoprotein cholesterol (HDL-C) in insulin resistance, such that improvement in insulin resistance decreases triglycerides and increases HDL-C. Patients with lipodystrophy have extreme insulin resistance with high

Reduction of abdominal obesity in lipodystrophy associated with human immunodeficiency virus infection by means of diet and exercise: case report and proof of principle.

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Lipodystrophy associated with human immunodeficiency virus infection causes abdominal fat gain, peripheral subcutaneous fat atrophy, insulin resistance, low levels of high-density lipoprotein cholesterol, and hypertriglyceridemia. An exercise program combined with a moderate-fat, low-glycemic-index,

Deletion of the serotonin 2c receptor from transgenic mice overexpressing leptin does not affect their lipodystrophy but exacerbates their diet-induced obesity.

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The binding of leptin to hypothalamic neurons elicits inhibition of orexigenic NPY/AgRP neurons and stimulation of anorexigenic POMC/CART neurons. Projections of serotonergic neurons onto POMC neurons suggest that leptin and serotonin converge onto POMC neurons to regulate body weight. We probed the
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