Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse

Preite, Nailliw Z.; Nascimento, Bruna Pascarelli Pedrico do; Muller, Cynthia R.; Américo, Anna Laura Viacava; Higa, Talita Sayuri; Evangelista, Fabiana S.; Lancellotti, Carmen Lúcia Penteado; Henriques, Felipe; Batista, M.; Bianco, Antonio C.; Ribeiro, Miriam O.

doi:10.1530/joe-16-0199

Cited by 30 publications

(21 citation statements)

References 45 publications

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“…Recent research shows intact BAT thermogenesis despite the lack of β3AR in β3ARKO mice. β3-AR is essential for lipolysis but not to brown adipose thermogenesis (Preite et al, 2016). In the present study, EA was found to increase the expression of the UCP1 and β3 adrenergic receptor in HFD rats.…”

Section: Discussionsupporting

confidence: 48%

Role of Neuro-Immune Cross-Talk in the Anti-obesity Effect of Electro-Acupuncture

Gong

et al. 2020

Front. Neurosci.

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There is evidence to show that electro-acupuncture (EA) has a promotive effect on both lipolysis and thermogenesis, and that these mechanisms underlie the anti-obesity effect of EA. The sympathetic nervous system (SNS) is known to play a role in thermogenesis. Additionally, obesity is characterized by a chronic low-grade inflammatory state. Based on these findings, the aim of the present study is to investigate the potential neuro-immune mechanisms underlying the therapeutic effect of EA in obesity. In the experiment, we used a high fat diet (HFD) rats model to study the effect of EA in reducing body weight. EA increases the activity of sympathetic nerves in inguinal white adipose tissue (iWAT), especially in the HFD group. Compared to HFD rats, EA can decrease sympathetic associated macrophage (SAM) and the level of norepinephrine transporter protein (Slc6a2). The relative uncoupling protein 1 expression shows EA increases thermogenesis in iWAT, and increases β3 receptors. Interestingly, injecting β antagonist in iWAT increases Slc6a2 protein levels. Additionally, the SNS-macrophage cross-talk response to EA showed in iWAT but not in epididymis white adipose tissue. The results of the present study indicate that EA exerts its anti-obesity effect via three mechanisms: (1) inhibition of SAMs and the norepinephrine transporter protein SlC6a2, (2) promoting SNS activity and thermogenesis, and (3) regulating immunologic balance.

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Section: Discussionsupporting

confidence: 48%

Role of Neuro-Immune Cross-Talk in the Anti-obesity Effect of Electro-Acupuncture

Gong

et al. 2020

Front. Neurosci.

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“…The ANS also influences local inflammatory responses in visceral and somatic tissues, via adrenergic and cholinergic receptor-mediated regulation of immune cells, connective tissue, and cardiovascular functioning. The ANS plays a major role in fat cell metabolism, vascular remodeling, and fibrosis associated with chronic inflammation [ 10 , 70 , 71 , 72 , 73 , 74 , 75 ]. The prevalence of chronic inflammation increases in frequency with advancing age, and may significantly contribute to premature aging, for which the term inflammaging has been coined [ 76 , 77 ].…”

Section: Autonomic Innervation Of the Spleen And Systemic Inflammamentioning

confidence: 99%

Sympathetic Nerve Hyperactivity in the Spleen: Causal for Nonpathogenic-Driven Chronic Immune-Mediated Inflammatory Diseases (IMIDs)?

Bellinger

Lorton

2018

IJMS

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Immune-Mediated Inflammatory Diseases (IMIDs) is a descriptive term coined for an eclectic group of diseases or conditions that share common inflammatory pathways, and for which there is no definitive etiology. IMIDs affect the elderly most severely, with many older individuals having two or more IMIDs. These diseases include, but are not limited to, type-1 diabetes, obesity, hypertension, chronic pulmonary disease, coronary heart disease, inflammatory bowel disease, and autoimmunity, such as rheumatoid arthritis (RA), Sjőgren’s syndrome, systemic lupus erythematosus, psoriasis, psoriatic arthritis, and multiple sclerosis. These diseases are ostensibly unrelated mechanistically, but increase in frequency with age and share chronic systemic inflammation, implicating major roles for the spleen. Chronic systemic and regional inflammation underlies the disease manifestations of IMIDs. Regional inflammation and immune dysfunction promotes targeted end organ tissue damage, whereas systemic inflammation increases morbidity and mortality by affecting multiple organ systems. Chronic inflammation and skewed dysregulated cell-mediated immune responses drive many of these age-related medical disorders. IMIDs are commonly autoimmune-mediated or suspected to be autoimmune diseases. Another shared feature is dysregulation of the autonomic nervous system and hypothalamic pituitary adrenal (HPA) axis. Here, we focus on dysautonomia. In many IMIDs, dysautonomia manifests as an imbalance in activity/reactivity of the sympathetic and parasympathetic divisions of the autonomic nervous system (ANS). These major autonomic pathways are essential for allostasis of the immune system, and regulating inflammatory processes and innate and adaptive immunity. Pathology in ANS is a hallmark and causal feature of all IMIDs. Chronic systemic inflammation comorbid with stress pathway dysregulation implicate neural-immune cross-talk in the etiology and pathophysiology of IMIDs. Using a rodent model of inflammatory arthritis as an IMID model, we report disease-specific maladaptive changes in β2-adrenergic receptor (AR) signaling from protein kinase A (PKA) to mitogen activated protein kinase (MAPK) pathways in the spleen. Beta2-AR signal “shutdown” in the spleen and switching from PKA to G-coupled protein receptor kinase (GRK) pathways in lymph node cells drives inflammation and disease advancement. Based on these findings and the existing literature in other IMIDs, we present and discuss relevant literature that support the hypothesis that unresolvable immune stimulation from chronic inflammation leads to a maladaptive disease-inducing and perpetuating sympathetic response in an attempt to maintain allostasis. Since the role of sympathetic dysfunction in IMIDs is best studied in RA and rodent models of RA, this IMID is the primary one used to evaluate data relevant to our hypothesis. Here, we review the relevant literature and discuss sympathetic dysfunction as a significant contributor to the pathophysiology of IMIDs, and then discuss a novel targ...

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“…There is reduced β3-AR mRNA expression in adipose tissue in non-pregnant offspring derived from diet-induced obese dams [28]. It was learned from β3-AR knockout mice that reductions in this signaling pathway increases the susceptibility to HFD-induced obesity [29]. It has also been demonstrated in humans that activation of β-AR signaling significantly reduces body weight and fat [30].…”

Section: Plos Onementioning

confidence: 99%

High-fat diet from parental generation exaggerates body and adipose tissue weights in pregnant offspring

Spradley

2020

PLoS ONE

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Parental high-fat diet (HFD) programs for obesity and hypertension in female offspring in rats, but it is unknown how the pregnancies of these offspring are impacted. Therefore, the hypothesis was tested that parental HFD exaggerates obesity and hypertension during pregnancy of the offspring. Wistar Hannover rat dams (the parental, P generation) were maintained on normal-fat diet (NFD) or HFD from weaning and were kept on respective diets through pregnancy and lactation. Their offspring (the first filial, F1 generation) were weaned onto the same diet as the P generation, or they were changed to the other diet to determine if combined HFD in the P and F1 generations exaggerates body weight and blood pressure levels during pregnancy in these offspring. This diet paradigm resulted in the following groups of pregnant F1 offspring: P-NFD/F1-NFD, P-HFD/F1-NFD, P-NFD/F1-HFD, and P-HFD/F1-HFD. Maternal body and adipose tissue weights were greatest in the P-HFD/F1-HFD group compared to the other 3 groups by the end of pregnancy. Plasma leptin and conscious mean arterial blood pressure were not significantly different between any group, although there was a main effect for increased blood pressure in the F1-HFD groups. Circulating levels of the antihypertensive pregnancy factor, placental growth factor (PlGF), were assessed. Although average PlGF levels were similar among all groups, correlative studies revealed that lower levels of PlGF were associated with higher blood pressure only in the P-HFD/F1-HFD group. In summary, HFD feeding from the P generation exaggerated HFD-induced body and adipose tissue weights in the pregnant offspring.

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Disruption of beta3 adrenergic receptor increases susceptibility to DIO in mouse

Cited by 30 publications

References 45 publications

Role of Neuro-Immune Cross-Talk in the Anti-obesity Effect of Electro-Acupuncture

Role of Neuro-Immune Cross-Talk in the Anti-obesity Effect of Electro-Acupuncture

Sympathetic Nerve Hyperactivity in the Spleen: Causal for Nonpathogenic-Driven Chronic Immune-Mediated Inflammatory Diseases (IMIDs)?

High-fat diet from parental generation exaggerates body and adipose tissue weights in pregnant offspring

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