Publications by authors named "Luiz Carlos Navegantes"

Despite the widespread use of L-3,4-dihydroxyphenylalanine (L-DOPA) as the gold standard for dopamine (DA) replacement in Parkinson's Disease (PD), its prolonged administration frequently leads to L-DOPA-induced dyskinesia (LID), a significant therapeutic challenge. Modulating the endocannabinoid system has emerged as a promising approach for managing LID. This study explored whether cannabidiol (CBD), a non-psychoactive compound of Cannabis sativa, and PECS-101, a fluorinated derivative of CBD, could mitigate the onset and progression of LID.

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Obesity is associated with the development of several illnesses, such as diabetes mellitus, cancer, and cardiovascular diseases. Elucidating the mechanisms of body weight control is important for the development of effective therapeutic strategies against obesity. In response to the action of hormones such as leptin and 17β-estradiol (E2), the ventromedial hypothalamus (VMH) plays an essential role in protection against diet-induced obesity (DIO) through the regulation of food intake and energy expenditure.

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Fibromyalgia (FM) is characterized by chronic widespread musculoskeletal pain accompanied by fatigue and muscle atrophy. Although its etiology is not known, studies have shown that FM patients exhibit altered function of the sympathetic nervous system (SNS), which regulates nociception and muscle plasticity. Nevertheless, the precise SNS-mediated mechanisms governing hyperalgesia and skeletal muscle atrophy in FM remain unclear.

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Although it is well established that fibromyalgia (FM) syndrome is characterized by chronic diffuse musculoskeletal hyperalgesia, very little is known about the effect of this pathology on muscle tissue plasticity. Therefore, the present study aimed to characterize the putative alterations in skeletal muscle mass in female rats subjected to a FM model by inducing chronic diffuse hyperalgesia (CDH) through double injections of acidic saline (pH 4.0) into the left gastrocnemius muscle at 5-day intervals.

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Although it has been previously demonstrated that oxytocin (OXT) receptor stimulation can control skeletal muscle mass in vivo, the intracellular mechanisms that mediate this effect are still poorly understood. Thus, rat oxidative skeletal muscles were isolated and incubated with OXT or WAY-267,464, a non-peptide selective OXT receptor (OXTR) agonist, in the presence or absence of atosiban (ATB), an OXTR antagonist, and overall proteolysis was evaluated. The results indicated that both OXT and WAY-267,464 suppressed muscle proteolysis, and this effect was blocked by the addition of ATB.

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Dietary restriction (DR) reduces adiposity and improves metabolism in patients with one or more symptoms of metabolic syndrome. Nonetheless, it remains elusive whether the benefits of DR in humans are mediated by calorie or nutrient restriction. This study was conducted to determine whether isocaloric dietary protein restriction is sufficient to confer the beneficial effects of dietary restriction in patients with metabolic syndrome.

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Aims: Although it is well established that skeletal muscle contains oxytocin (OT) receptors and OT-knockout mice show premature development of sarcopenia, the role of OT in controlling skeletal muscle mass is still unknown. Therefore, the present work aimed to determine OT's effects on skeletal muscle protein metabolism.

Main Methods: Total proteolysis, proteolytic system activities and protein synthesis were assessed in isolated soleus muscle from prepubertal female rats.

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Article Synopsis
  • The study aimed to evaluate the effects of a low-protein diet (6% protein) versus a normal-protein diet (17%) on growing rats over 15 days.
  • Results showed that rats on the low-protein diet were hyperphagic (ate more) and had increased energy expenditure, but also experienced poor growth and changes in body composition, such as higher fat content.
  • The findings suggest a potential resistance to leptin and an increase in insulin sensitivity, indicating complex metabolic responses to protein restriction despite higher caloric intake and energy expenditure.
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Background: Long periods of ischemia can cause organ injury and dysfunction. The protein degradation occurring in the muscular layer and in the mucosa of the intestinal wall during ischemia may release amino acids into the intestinal lumen or into the circulation. The small intestine, like skeletal muscle, cannot synthesize or degrade tyrosine.

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