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Morphometric analysis of obesity (ob/ob)- and diabetes (db/db)-associated hypothalamic neuronal degeneration in C57BL/KsJ mice.
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The influence of the obese (ob/ob) and diabetes (db/db) genetic mutations on hypothalamic structure was investigated in C57BL/KsJ and C57BL/6J mice strains by morphometric analysis of medial basal nuclei which are recognized to possess glucoregulatory neurons. Brains were collected and prepared for
Ladder-Climbing Training Prevents Bone Loss and Microarchitecture Deterioration in Diet-Induced Obese Rats.
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Resistance exercise has been proved to be effective in improving bone quality in both animal and human studies. However, the issue about whether resistance exercise can inhibit obesity-induced bone loss has not been previously investigated. In the present study, we have evaluated the effects of
Obesity-induced type 2 diabetes impairs neurological recovery after stroke in correlation with decreased neurogenesis and persistent atrophy of parvalbumin-positive interneurons.
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Type 2 diabetes (T2D) hampers stroke recovery though largely undetermined mechanisms. Few preclinical studies have investigated the effect of genetic/toxin-induced diabetes on long-term stroke recovery. However, the effects of obesity-induced T2D are mostly unknown. We aimed to investigate whether
Predictors of deterioration of glucose tolerance and effects of lifestyle intervention aimed at reducing visceral fat in normal glucose tolerance subjects with abdominal obesity.
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Aims/Introduction: The aim of the present study was to determine the predictors of deterioration of glucose tolerance in individuals with normal glucose tolerance (NGT) and abdominal obesity, and whether a lifestyle intervention to reduce visceral fat is effective in these individuals.
METHODS
The
Does obesity exacerbate brain lesion volume and atrophy in patients with multiple sclerosis?
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Background: Obesity is common among patients with multiple sclerosis (pwMS) and has been shown to exacerbate central inflammation, a key factor in disease progression. The purpose of this cross-sectional study is to examine the possible
Altered dipeptidyl peptidase-4 activity during the progression of hyperinsulinemic obesity and islet atrophy in spontaneously late-stage type 2 diabetic rats.
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Altered dipeptidyl peptidase-4 (DPP4) activity during the progression of late-stage type 2 diabetes was measured in Otsuka Long-Evans Tokushima fatty (OLETF) rats. Compared with OLETF rats subjected to 30% food restriction, food-satiated OLETF rats exhibited spontaneous hyperphagic obesity, insulin
Impact of obesity with impaired glucose tolerance on retinal degeneration in a rat model of metabolic syndrome.
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Metabolic syndrome (MetS) is associated with several degenerative diseases, including retinal degeneration. Previously, we reported on progressive retinal degeneration in a spontaneous obese rat (WNIN/Ob) model. In this study, we investigated the additional effect of impaired glucose tolerance
High-fat/high-sucrose diet-induced obesity results in joint-specific development of osteoarthritis-like degeneration in a rat model.
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UNASSIGNED
Metabolic syndrome and low-grade systemic inflammation are associated with knee osteoarthritis (OA), but the relationships between these factors and OA in other synovial joints are unclear. The aim of this study was to determine if a high-fat/high-sucrose (HFS) diet results in OA-like
Association study between the polymorphisms of the fat mass- and obesity-associated gene with the risk of intervertebral disc degeneration in the Han Chinese population.
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OBJECTIVE
Insights gained from studies suggest that genetic factors are major contributors to the onset and progression of intervertebral disc degeneration (IVDD). The aim of this study is to investigate whether fat mass- and obesity-associated (FTO) gene polymorphisms are related to the disease in
Deletion of Thioredoxin-Interacting Protein (TXNIP) Abrogates High Fat Diet-induced Retinal Leukostasis, Barrier Dysfunction and Microvascular Degeneration in a Mouse Obesity Model
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We have shown that a high fat diet (HFD) induces the activation of retinal NOD-like receptor protein (NLRP3)-inflammasome that is associated with enhanced expression and interaction with thioredoxin-interacting protein (TXNIP). Here, the specific contribution of TXNIP and the impact of HFD on
One-hour glucose during an oral glucose challenge prospectively predicts β-cell deterioration and prediabetes in obese Hispanic youth.
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OBJECTIVE
In adults, 1-h glucose during an oral glucose tolerance test (OGTT) predicts the development of type 2 diabetes independent of fasting and 2-h glucose concentrations. The purpose of the current investigation was to examine the utility of elevated 1-h glucose levels to prospectively predict
Quantitative histopathological assessment of retardation of islets of langerhans degeneration in rosiglitazone-dosed obese ZDF rats using combined insulin and collagens (I and III) immunohistochemistry with automated image analysis and statistical modeling.
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Islets of Langerhans represent a heterogeneous population in insulin resistant and diabetic animals and humans as histological appearances and function vary substantially. Mathematical representation that reflects this morphological diversity will assist in assessment of degeneration and
Obesity Mediates Apoptosis and Extracellular Matrix Metabolic Imbalances via MAPK Pathway Activation in Intervertebral Disk Degeneration.
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Obesity may promote intervertebral disc degeneration (IDD) by non-mechanical means, by influencing levels of free fatty acids which could impair cell metabolism. This study aims to establish metabolic factors in obesity-related IDD independent of mechanical loading. In clinical study, we
A novel rat model with obesity-associated retinal degeneration.
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OBJECTIVE
A strong association between retinal degeneration and obesity has been shown in humans. However, the molecular basis of increased risk for retinal degeneration in obesity is unknown. Thus, an animal model with obesity and retinal degeneration would greatly aid the understanding of
Severe thyroid atrophy due to prolonged ingestion of thyroid hormone for treatment of obesity.
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Severe thyroid atrophy was found at the autopsy of a 39-year-old white woman who died of myocarditis, probably of viral etiology. Prolonged ingestion of thyroid hormone for the treatment of obesity appears to be the only plausible explanation for the atrophy, secondary to suppression of the
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