Adipose proinflammatory cytokine expression through sympathetic system is associated with hyperglycemia and insulin resistance in a rat ischemic stroke model

Wang, Yayu; Lin, Shih‐Yi; Chuang, Yu Han; Chen, Chun‐Jung; Tung, Kwong‐Chung; Sheu, Wayne Huey‐Herng

doi:10.1152/ajpendo.00301.2010

Cited by 64 publications

(50 citation statements)

References 44 publications

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“…Independent of obesity, hypothalamic inflammation can impair insulin release from β cells, impair peripheral insulin action, and potentiate hypertension (63-65). Many of these effects are generated by signals from the sympathetic nervous system, which is also capable of inducing inflammatory changes in adipose tissue in response to neuronal injury (66). A future challenge is to understand how inflammatory signals in the brain generate responses that in some cases generate negative energy balance (anorexia), while in other cases generates positive energy balance (weight gain) (67).…”

Section: Figurementioning

confidence: 99%

Inflammatory links between obesity and metabolic disease

Lumeng¹,

Saltiel²

2011

J. Clin. Invest.

1,885

1,494

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The obesity epidemic has forced us to evaluate the role of inflammation in the health complications of obesity. This has led to a convergence of the fields of immunology and nutrient physiology and the understanding that they are inextricably linked. The reframing of obesity as an inflammatory condition has had a wide impact on our conceptualization of obesity-associated diseases. In this Review, we highlight the cellular and molecular mechanisms at play in the generation of obesity-induced inflammation. We also emphasize how defining the immune regulation in metabolic tissues has broadened the understanding of the diversity of inflammatory responses. IntroductionThe burden of obesity on health extends across multiple organ systems and diseases. While its impact on tissues involved in nutrient regulation is manifest in the development of insulin resistance and type 2 diabetes, there are also unexpected connections between obesity and the risk of cancer and pulmonary diseases. Over the past decade, the search for a potential unifying mechanism behind the pathogenesis of obesity-associated diseases has revealed a close relationship between nutrient excess and derangements in the cellular and molecular mediators of immunity and inflammation. This has given birth to the concept of "metainflammation" (1) to describe the chronic low-grade inflammatory response to obesity. We present here a broad overview of the links between obesity and immune responses with a focus on metabolic disease and argue that the intersection between the pathways that control nutrient metabolism and inflammatory responses may be broadly applicable to our understanding of inflammation and the immune system.

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Section: Figurementioning

confidence: 99%

Inflammatory links between obesity and metabolic disease

Lumeng¹,

Saltiel²

2011

J. Clin. Invest.

1,885

1,494

View full text Add to dashboard Cite

show abstract

“…injection of glucose (2 g/kg). Blood samples were taken from the tail vein, and glucose was measured using commercially available kits (Wiener Lab, Argentina) at 0 (fasting), 30, 60, 90 and 120 minutes after glucose administration (Wang et al, 2011). The total area under curve (AUC) for glucose during the ipGTT (2-h glucose area under curve) was calculated using Origin software (Origin, Origin Lab Corporation, MA USA).…”

Section: Intraperitoneal Glucose Tolerance Test (Ipgtt)mentioning

confidence: 99%

Withdrawal of dietary phytoestrogens in adult male rats affects hypothalamic regulation of food intake, induces obesity and alters glucose metabolism

Andreoli

Stoker

Rossetti

et al. 2015

Molecular and Cellular Endocrinology

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A B S T R A C TThe absence of phytoestrogens in the diet during pregnancy has been reported to result in obesity later in adulthood. We investigated whether phytoestrogen withdrawal in adult life could alter the hypothalamic signals that regulate food intake and affect body weight and glucose homeostasis.Male Wistar rats fed from conception to adulthood with a high phytoestrogen diet were submitted to phytoestrogen withdrawal by feeding a low phytoestrogen diet, or a high phytoestrogen-high fat diet. Withdrawal of dietary phytoestrogens increased body weight, adiposity and energy intake through an orexigenic hypothalamic response characterized by upregulation of AGRP and downregulation of POMC. This was associated with elevated leptin and T4, reduced TSH, testosterone and estradiol, and diminished hypothalamic ERα expression, concomitant with alterations in glucose tolerance.Removing dietary phytoestrogens caused manifestations of obesity and diabetes that were more pronounced than those induced by the high phytoestrogen-high fat diet intake.

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“…Through the repetitive hypoxia-reoxygenation sequence, intermittent hypoxia generates free radical stress and inflammation. Intermittent hypoxia also increases sympathoadrenergic activity, which in turn exacerbates oxidative stress [21], and the adipose expression of MCP-1 [22], which is a key chemokine regulating macrophage tissue infiltration [23]. We used isoprenaline to mimic the sympathetic overactivity occuring in OSA patients during sleep, which resulted in enhanced proinflammatory cytokine release.…”

Section: Intermittent Hypoxia Induces Ewat Remodellingmentioning

confidence: 99%

Visceral white fat remodelling contributes to intermittent hypoxia-induced atherogenesis

Poulain

Thomas

Rieusset

et al. 2013

European Respiratory Journal

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Obstructive sleep apnoea is a highly prevalent disease characterised by repetitive upper airway collapse during sleep leading to intermittent hypoxia. Cardiometabolic complications of sleep apnoea have been mostly attributed to intermittent hypoxia. These consequences could be mediated through intermittent hypoxia-related alterations of the visceral white fat, as it is recognised for playing an important role in inflammation, atherogenesis and insulin resistance.Epididymal adipose tissue alterations were investigated in 20-week-old nonobese male apolipoprotein Edeficient mice exposed to intermittent hypoxia (inspiratory oxygen fraction 5-21%, 60-s cycle, 8 h?day -1 ) or air for 6 weeks. These adipose tissue alterations, as well as metabolic alterations and aortic atherosclerosis, were then assessed in lipectomised or sham-operated mice exposed to intermittent hypoxia or air for 6 weeks.Intermittent hypoxia induced morphological (shrunken adipocytes), functional (increased uncoupling protein-1 expression) and inflammatory (increased macrophage recruitment and secretion of interleukin-6 and tumour necrosis factor-a) remodelling of epididymal adipose tissue. Hypoxic mice presented more severe dyslipidaemia and atherosclerosis lesions and developed insulin resistance. Epididymal lipectomy attenuated both intermittent hypoxia-induced dyslipidaemia and atherogenesis, but did not improve insulin sensitivity.Our results confirmed that the dyslipidaemic and proatherogenic effects of intermittent hypoxia are partly mediated through morphological, functional and inflammatory remodelling of visceral white fat, regardless of obesity. @ERSpublications Dyslipidaemic and proatherogenic effects of intermittent hypoxia are partly mediated by visceral white fat remodelling

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Adipose proinflammatory cytokine expression through sympathetic system is associated with hyperglycemia and insulin resistance in a rat ischemic stroke model

Cited by 64 publications

References 44 publications

Inflammatory links between obesity and metabolic disease

Inflammatory links between obesity and metabolic disease

Withdrawal of dietary phytoestrogens in adult male rats affects hypothalamic regulation of food intake, induces obesity and alters glucose metabolism

Visceral white fat remodelling contributes to intermittent hypoxia-induced atherogenesis

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