Integrative neurobiology of energy homeostasis-neurocircuits, signals and mediators

Sánchez-Lasheras, Carmen; Könner, A. Christine; Brüning, Jens C.

doi:10.1016/j.yfrne.2009.08.002

Cited by 97 publications

(84 citation statements)

References 206 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Hepatic glycogen levels were measured with glycogen assay kits (BioVision, Mountain View, CA) (14). Plasma [3-H 3 ] glucose-specific activity was measured in duplicates in the supernatants of Ba (OH) 2 and ZnSO 4 precipitates (Somogyi procedure) of plasma samples after evaporation to dryness to eliminated tritiated water. Under steady-state conditions, the rate of glucose disappearance (GRd) equals the rate of glucose appearance.…”

Section: Analytical Proceduresmentioning

confidence: 99%

Hypothalamic Nesfatin-1/NUCB2 Knockdown Augments Hepatic Gluconeogenesis That Is Correlated With Inhibition of mTOR-STAT3 Signaling Pathway in Rats

Yang

Chen

et al. 2014

Diabetes

View full text Add to dashboard Cite

Nesfatin-1, an 82-amino acid neuropeptide, has recently been characterized as a potent metabolic regulator. However, the metabolic mechanisms and signaling steps directly associated with the action of nesfatin-1 have not been well delineated. We established a loss-of-function model of hypothalamic nesfatin-1/NUCB2 signaling in rats through an adenoviral-mediated RNA interference. With this model, we found that inhibition of central nesfatin-1/NUCB2 activity markedly increased food intake and hepatic glucose flux and decreased glucose uptake in peripheral tissue in rats fed either a normal chow diet (NCD) or a highfat diet (HFD). The change of hepatic glucose fluxes in the hypothalamic nesfatin-1/NUCB2 knockdown rats was accompanied by increased hepatic levels of glucose-6-phosphatase and PEPCK and decreased insulin receptor, insulin receptor substrate 1, and AKT kinase phosphorylation. Furthermore, knockdown of hypothalamic nesfatin-1 led to decreased phosphorylation of mammalian target of rapamycin (mTOR) and signal transducer and activator of transcription 3 (STAT3) and the subsequent suppressor of cytokine signaling 3 levels. These results demonstrate that hypothalamic nesfatin-1/NUCB2 plays an important role in glucose homeostasis and hepatic insulin sensitivity, which is, at least in part, associated with the activation of the mTOR-STAT3 signaling pathway. Diabetes 2014;63:123463: -124763: | DOI: 10.2337 The hypothalamus, where numerous neuropeptides and transmitters are released to control essential body functions, has been considered a key integrator in the central control of food intake and energy balance (1,2). Oh-I et al. (3) discovered nesfatin-1, an 82-amino acid polypeptide, while searching for new appetite-controlling signals. Nesfatin-1 is the cleavage product of the calcium and DNA-binding protein nucleobindin2 (NUCB2),

show abstract

Section: Analytical Proceduresmentioning

confidence: 99%

Hypothalamic Nesfatin-1/NUCB2 Knockdown Augments Hepatic Gluconeogenesis That Is Correlated With Inhibition of mTOR-STAT3 Signaling Pathway in Rats

Yang

Chen

et al. 2014

Diabetes

View full text Add to dashboard Cite

show abstract

“…Among those, considerable efforts have been devoted recently to unveil the complex circuitries and regulatory factors involved in the central control of food intake and energy balance (Stanley et al 2005, Sanchez-Lasheras et al 2010. Unraveling of these pathways and signals is not only physiologically relevant but also poses obvious pharmacological implications, as basis for the rational design of improved therapeutic strategies for the control of body weight, whose disorders (ranging from obesity to anorexia) have grown in prevalence to epidemic proportions in recent years.…”

Section: Identification and Structural Biology Of Nesfatin-1mentioning

confidence: 99%

Expanding roles of NUCB2/nesfatin-1 in neuroendocrine regulation

García-Galiano

Navarro

Gaytán

et al. 2010

Journal of Molecular Endocrinology

120

View full text Add to dashboard Cite

Nesfatin-1 was originally identified as a hypothalamic neuropeptide, derived from the precursor NEFA (for DNA binding/EF-hand/acidic protein)/nucleobindin 2 (NUCB2), with the ability to suppress food intake, acting in a leptin-independent manner. Departing from this seminal finding, the patterns of expression of NUCB2/nesfatin-1 have been thoroughly characterized in different hypothalamic nuclei and brain areas with proven roles in energy homeostasis, and its potential interactions with other key neuropeptide regulators of appetite have been documented. Intriguingly, recent experimental evidence suggests that NUCB2/nesfatin-1 is also expressed in peripheral tissues with relevant metabolic functions, such as the pancreas, the adipose, and the gut. In addition, evidence is mounting that nesfatin signaling may participate in adaptative responses and in the control of body functions gated by the state of energy reserves, such as puberty onset. Altogether, these observations have broadened our perception of the biological profile of nesfatin-1 that, rather than a simple anorectic signal in the hypothalamus, might operate at different tissues as an integral regulator of energy homeostasis and closely related neuroendocrine functions.

show abstract

“…Los efectos de las dietas hipercalóricas han sido ampliamente estudiados y relacionadas con la obesidad y otras patologías como las hiperlipidemias; en este estudio, los resultados de los grupos de ratas que recibieron una dieta hipercalórica no son la excepción: las ratas de los grupos GH y GH+GlcN tuvieron un aumento y ganancia de peso corporal ( Figura 1A y B), aunque el consumo energético fue similar a los grupos con dieta normal GC y GGlcN; se ha reportado que la ingestión de grasas ha sido el eje del aumento de peso, por la interrelación compleja de factores como el apetito, la ingesta, la absorción de nutrimentos, reguladores neuroendocrinos, formas de almacenamiento de energía y gasto energético total, siendo la grasa un nutriente que se correlaciona positivamente con el aumento de peso 26 y que se corresponde directamente con el aumento de la cantidad de grasa abdominal, efectos también observados para los grupos GH y GH+GlcN (Figura 2A). En este estudio, se ha descrito que, cuando el porcentaje de grasa en la dieta es elevado, se produce un desequilibrio entre la ingesta y la oxidación de la grasa que conduce a un aumento en el tamaño del tejido adiposo, hasta que los adipocitos se vuelven hipertróficos e hiperplásicos.…”

Section: I S C U S I ó Nunclassified

Efecto de la administración subcrónica de glucosamina oral en la regulación del peso corporal, glucemia y dislipidemias provocada por una dieta hipercalórica en rata Wistar

Barrientos‐Alvarado

Vázquez²,

Oscoy³

et al. 2014

Rev. Nutr.

View full text Add to dashboard Cite

ObjetivoEste estudio evaluó el efecto de la glucosamina oral en el sobrepeso y dislipidemia provocada por una dieta hipercalórica en ratas. MétodosEn 4 grupos de ratas Wistar: alimentados con dieta comercial para roedores y agua de beber sin grupo de control y con glucosamina (500 mg/kg-1 por día) grupo glucosamina y con dieta hipercalórica enriquecida al 24% (g/g) compuesta por manteca de cerdo y agua de beber sin grupo hipercalórico y con glucosamina grupo hipercalórico + grupo glucosamina, durante 22 semanas, se evaluaron el peso corporal, grasa abdominal, niveles de glucemia, triglicéridos, colesterol total y lipoproteínas de alta densidad en suero. ResultadosSe observó un aumento del peso corporal y glucemia en suero con dislipidemias en el grupo con dieta hipercalórica grupo hipercalórico versus grupo de controle (p<0.001); al administrarse glucosamina para esta misma dieta grupo hipercalórico + grupo glucosamina se minimizaron los efectos presentados, disminuyendo la cantidad de grasa abdominal y los niveles del perfil lípido en suero (p>0.05) y regulándose el peso corporal, las lipoproteínas de alta densidad y la glucemia basal (p<0.05). ConclusionLa glucosamina reguló el peso corporal y la glucemia en sangre y minimizó las dislipidemias provocadas por la dieta hipercalórica, favoreciendo el aumento de colesterol lipoproteínas de alta densidad en las ratas. No afectó el peso corporal y el metabolismo lipídico cuando se administró con dieta comercial.Palabras ilave: Glucemia. Glucosamina. HDL-colesterol. Peso corporal. A B S T R A C T Objective This study evaluated the effect of oral glucosamine on overweight and dyslipidemia caused by a high-fat diet in rats. Methods Four groups of Wistar rats: fed with commercial rodent food and drinking water without (control group) and with glucosamine (500 mg kg-1 per day) and a high-fat diet enriched with 24% (g/g) butter pork and drinking water without and with glucosamine, for 22 weeks; the body weight, abdominal fat, blood glucose, triglycerides, total cholesterol, and high density lipoprotein in serum were evaluated. Results Body

show abstract

Integrative neurobiology of energy homeostasis-neurocircuits, signals and mediators

Cited by 97 publications

References 206 publications

Hypothalamic Nesfatin-1/NUCB2 Knockdown Augments Hepatic Gluconeogenesis That Is Correlated With Inhibition of mTOR-STAT3 Signaling Pathway in Rats

Hypothalamic Nesfatin-1/NUCB2 Knockdown Augments Hepatic Gluconeogenesis That Is Correlated With Inhibition of mTOR-STAT3 Signaling Pathway in Rats

Expanding roles of NUCB2/nesfatin-1 in neuroendocrine regulation

Efecto de la administración subcrónica de glucosamina oral en la regulación del peso corporal, glucemia y dislipidemias provocada por una dieta hipercalórica en rata Wistar

Contact Info

Product

Resources

About