Faculty Opinions recommendation of Hypothalamic IKKbeta/NF-kappaB and ER stress link overnutrition to energy imbalance and obesity.

By Y. Loh. 2008

701 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/f4713d4916519b02d1c59c5d42d58f8ed0abf62c

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Citations in the corpus

Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer (2009, background): “Functional interaction or antagonism between NF-κB and STAT3 can also occur at the level of signal transduction regulators, such as SOCS proteins whose expression is controlled by both NF-κB and STAT3 (42,67,68).”
Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, unknown): “However, recent studies in the brain provide in vivo evidence supporting the model that both ER stress and inflammation are able to activate each other and to inhibit normal cellular metabolism (Zhang et al., 2008).”
Inflammation, Defective Insulin Signaling, and Mitochondrial Dysfunction as Common Molecular Denominators Connecting Type 2 Diabetes to Alzheimer Disease (2014, background): “In animal models of T2D and obesity, an inflammatory response in the hypothalamus, notably via activation of TNF-a and the IkBa kinase (IKK)-b/nuclear factor-kB pathway, is an important part of the mechanism underlying pathogenesis (69,70).”
Lipid-induced insulin resistance mediated by the proinflammatory receptor TLR4 requires saturated fatty acid-induced ceramide biosynthesis in mice. (2011, result): “org Volume 121 Number 5 May 2011 mediating onset of obesity (47), but we did not observe a statistically significant divergence in body weight in high-fat diet–fed animals treated with or without NS, a finding corroborated by others (53).”
Understanding the somatic consequences of depression: biological mechanisms and the role of depression symptom profile (2013, background): “In the central nervous system obesity-associated inflammation can disrupt leptin hypothalamic action through IKKβ/NFkβ regulation of SOCS-3 (suppressor of cytokine signaling-3), a key inhibitor of leptin signaling [67].”
Adipokines Mediate Inflammation and Insulin Resistance (2013, background): “More recently, amlexanox, an inhibitor of the non-canonical IκB kinases IKK-ε and TANKbinding kinase 1 (TBK1) was shown to not only improve sensitivity but to also increase energy expenditure and weight loss in obese mice (Reilly et al., 2013).”