Altered sciatic nerve fiber morphology and endoneural microvessels in mouse models relevant for obesity, peripheral diabetic polyneuropathy, and the metabolic syndrome

2011 ◽  
Vol 90 (1) ◽  
pp. 122-131 ◽  
Author(s):  
Marcin Nowicki ◽  
Joanna Kosacka ◽  
Heike Serke ◽  
Matthias Blüher ◽  
Katharina Spanel-Borowski
Keyword(s):  
Metabolic Syndrome ◽  
Sciatic Nerve ◽  
Nerve Fiber ◽  
Mouse Models ◽  
Diabetic Polyneuropathy ◽  
Fiber Morphology ◽  
The Metabolic Syndrome

scholarly journals Mouse models of lipodystrophy: Key reagents for the understanding of the metabolic syndrome

2007 ◽  
Vol 4 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Ingrid Wernstedt Asterholm ◽  
Nils Halberg ◽  
Philipp E. Scherer
Keyword(s):  
Metabolic Syndrome ◽  
Mouse Models ◽  
The Metabolic Syndrome

scholarly journals Mouse models of the metabolic syndrome

2010 ◽  
Vol 3 (3-4) ◽  
pp. 156-166 ◽  
Author(s):  
A. J. Kennedy ◽  
K. L. J. Ellacott ◽  
V. L. King ◽  
A. H. Hasty
Keyword(s):  
Metabolic Syndrome ◽  
Mouse Models ◽  
The Metabolic Syndrome

Mouse models of PPAR-γ deficiency: dissecting PPAR-γ's role in metabolic homoeostasis

2005 ◽  
Vol 33 (5) ◽  
pp. 1053-1058 ◽  
Author(s):  
S.L. Gray ◽  
E. Dalla Nora ◽  
A.J. Vidal-Puig
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Adipose Tissue ◽  
Mouse Models ◽  
Murine Models ◽  
Metabolic Processes ◽  
Glucose Homoeostasis ◽  
Ppar Γ ◽  
The Metabolic Syndrome

The identification of humans with mutations in PPAR-γ (peroxisome-proliferator-activated receptor-γ) has underlined its importance in the pathogenesis of the metabolic syndrome. Genetically modified mice provide powerful tools to dissect the mechanisms by which PPAR-γ regulates metabolic processes. Ablation of PPAR-γ in vivo is lethal and thus dissection of PPAR-γ function using mouse models has relied on the development of tissue and isoform-specific ablation and mouse models of human mutations. These models exhibit phenotypes of partial PPAR-γ impairment and are useful to elucidate how PPAR-γ regulates specific metabolic processes. These murine models have confirmed the involvement of PPAR-γ in adipose tissue development, maintenance and distribution. The mechanism involved in PPAR-γ regulation of glucose homoeostasis is obscure as both agonism and partial impairment of PPAR-γ increase insulin sensitivity. While adipose tissue is likely to be the primary target for the insulin-sensitizing effects of PPAR-γ, some murine models suggest PPAR-γ expressed outside adipose tissue may also contribute actively to maintain glucose homoeostasis. Interestingly, mutations in PPAR-γ that cause severe insulin resistance in humans when expressed in mice do not result in insulin insensitivity. However, these murine models can recapitulate the effects in fuel partitioning, post-prandial lipid handling and vasculature dysfunction observed in humans. In summary, these murine models of PPAR-γ have provided useful in vivo systems to dissect the function of PPAR-γ, but additionally have revealed a picture of complexity. These models have confirmed a key role for PPAR-γ in the metabolic syndrome; however, they challenge the concept that insulin resistance is the main factor linking the clinical manifestations of the metabolic syndrome.

scholarly journals Insulin signaling, resistance, and metabolic syndrome: insights from mouse models into disease mechanisms

2013 ◽  
Vol 220 (2) ◽  
pp. T1-T23 ◽  
Author(s):  
Shaodong Guo
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Mouse Models ◽  
Insulin Signaling ◽  
Control Cell ◽  
Significant Risk ◽  
Significant Risk Factor ◽  
Signaling Cascade ◽  
Metabolic Inflammation ◽  
The Metabolic Syndrome

Insulin resistance is a major underlying mechanism responsible for the ‘metabolic syndrome’, which is also known as insulin resistance syndrome. The incidence of metabolic syndrome is increasing at an alarming rate, becoming a major public and clinical problem worldwide. Metabolic syndrome is represented by a group of interrelated disorders, including obesity, hyperglycemia, hyperlipidemia, and hypertension. It is also a significant risk factor for cardiovascular disease and increased morbidity and mortality. Animal studies have demonstrated that insulin and its signaling cascade normally control cell growth, metabolism, and survival through the activation of MAPKs and activation of phosphatidylinositide-3-kinase (PI3K), in which the activation of PI3K associated with insulin receptor substrate 1 (IRS1) and IRS2 and subsequent Akt→Foxo1 phosphorylation cascade has a central role in the control of nutrient homeostasis and organ survival. The inactivation of Akt and activation of Foxo1, through the suppression IRS1 and IRS2 in different organs following hyperinsulinemia, metabolic inflammation, and overnutrition, may act as the underlying mechanisms for metabolic syndrome in humans. Targeting the IRS→Akt→Foxo1 signaling cascade will probably provide a strategy for therapeutic intervention in the treatment of type 2 diabetes and its complications. This review discusses the basis of insulin signaling, insulin resistance in different mouse models, and how a deficiency of insulin signaling components in different organs contributes to the features of metabolic syndrome. Emphasis is placed on the role of IRS1, IRS2, and associated signaling pathways that are coupled to Akt and the forkhead/winged helix transcription factor Foxo1.

1237: Erectile Dysfunction (ED) Evaluation Through the Metabolic Syndrome Window

2005 ◽  
Vol 173 (4S) ◽  
pp. 335-336 ◽  
Author(s):  
Omer Demir ◽  
Tevfik Demir ◽  
Aykut Kefi ◽  
Abdurrahman Comlekci ◽  
Sena Yesil ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Erectile Dysfunction ◽  
The Metabolic Syndrome
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