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LPS leads to an increase in SOCS3 expression [20]. SOCS3 is a negative regulator of leptin signaling

We observed a significant increase in energy intake in the LPS-treated rats

the data provides a mechanism linking changes in gut microbiota induced by ingestion of HF diets to dysregulation of food intake and body weight

SOCS3 is an important mechanism by which leptin resistance develops in vagal afferent neurons and coincides with the onset of hyperphagia

Chronic low-dose LPS treatment induced TLR4 activation and MyD88 signaling in vagal afferent neurons, associated with increased SOCS3 expression and reduced leptin-signaling, characterized by the absence of leptin-induced pSTAT3.

We demonstrate that this chronic low dose LPS is sufficient to induce leptin–resistance in vagal afferent neurons, reduced sensitivity to the satiating effects of CCK, and loss of vagal afferent plasticity

it suggests that the increase in food intake and body weight we observed at week 6 in the LPS treated rats may be caused by LPS-induced leptin resistance.

chronic LPS treatment of mice for four weeks increased body weight

chronic LPS treatment of mice for four weeks increased subcutaneous fat

Recent evidence suggests that the eNOS/NO/cGMP pathway is an important activator of mitochondrial biogenesis

BH4 (tetrahydrobiopterin) supplementation can prevent eNOS uncoupling and was found to reduce left ventricular hypertrophy

folic acid is known to replenish reduced BH4 and has been shown to protect the heart through increased eNOS activity

Both folate deficiency and inhibition of BH4 synthesis were associated with reduced mitochondrial number and function

Resveratrol, a polyphenol compound responsible for the cardioprotective properties of red wine, was recently identified as a potent stimulator of mitochondrial biogenesis

epidemiological studies reveal a reduced risk of cardiovascular disease in premenopausal, but not post-menopausal, women compared with men

post-menopausal women

The majority of ROS in the heart appear to come from uncoupling of mitochondrial electron transport chain at the level of complexes I and III

Because the majority of ROS in HF comes from mitochondria, these organelles are the primary target of oxidative damage.

cardioprotective therapies such as angiotensin-converting enzyme inhibitors and ATII receptor blockers were shown to possess antioxidant properties, although it is not known whether they target mitochondrial ROS directly or indirectly

(SOCS)-3. A member of a protein family originally characterized as negative feedback regulators of inflammation (13, 37), SOCS3 inhibits insulin and leptin signaling

IKKβ signaling in discrete neuronal subsets appears to be required for both hypothalamic inflammation and excess weight gain to occur during HF feeding

the paradoxical observation that hyperphagia and weight gain occur when hypothalamic inflammation is induced by HF feeding, yet when it occurs in response to systemic or local inflammatory processes (e.g. administration of endotoxin), anorexia and weight loss are the rule

, serves as a circulating signal of energy stores in part by providing feedback inhibition of hypothalamic orexigenic pathways [e.g. neurons that express neuropeptide Y and agouti-related peptide (AgRP)]

and stimulating anorexigenic neurons

signals from Toll-like receptors (TLRs), evolutionarily conserved pattern recognition molecules critical for detecting pathogens, amplified through signaling intermediates such as MyD88 activate the inhibitor of κB-kinase-β (IKKβ)/nuclear factor-κB (NF-κB), c-Jun N-terminal kinase (Jnk) and other intracellular inflammatory signals in response to stimulation by circulating saturated fatty acids

During the I/R period, testosterone replacement in ORX rats exerted the beneficial effects as indicated by (1) improved left ventricular pressure; (2) markedly decreased infarct size; (3) reduced fatal cardiac arrhythmias by increased time to 1st VT/VF onset and reduced arrhythmia scores; and (4) attenuated cardiac mitochondrial dysfunction caused by I/R injury by reducing ROS production, cardiac mitochondrial swelling and mitochondria membrane depolarization.

Chronic testosterone replacement also ameliorates left ventricular dysfunction, and reduces the infarct size and cardiac arrhythmias impaired by I/R injury under testosterone-deprived conditions

The mechanisms responsible for these beneficial effects of testosterone could be due to its ability to attenuate cardiac mitochondrial dysfunction and cardiomyocyte apoptosis

FT3 levels were inversely correlated to coronary artery disease