Vagus nerve damage increases alcohol intake and preference in a nonpreferring rat line: Relationship to vagal regulation of the hypothalamic-pituitary-adrenal axis.

Background: Clinical and preclinical research indicates that gastric weight loss surgeries, such as Roux-en-Y gastric bypass surgery, can induce alcohol use disorder (AUD). While numerous mechanisms have been proposed for these effects, one relatively unexplored potential mechanism is physical damage to the gastric branch of the vagus nerve, which can occur during bypass surgery. Therefore, we hypothesized that direct damage to the gastric branch of the vagus nerve, without altering other aspects of gastric anatomy, could result in increased alcohol intake.

Adolescent alcohol disrupts development of noradrenergic neurons in the nucleus of the tractus solitarius and enhances stress behaviors in adulthood in mice in a sex specific manner.

Alcohol use disorders (AUDs) are common mental health issues worldwide and can lead to other chronic diseases. Stress is a major factor in the development and continuation of AUDs, and adolescent alcohol exposure can lead to enhanced stress-responsivity and increased risk for AUD development in adulthood. The exact mechanisms behind the interaction between adolescence, stress, and alcohol are not fully understood and require further research.

Minocycline Reduces Hypothalamic Microglia Activation and Improves Metabolic Dysfunction in High Fat Diet-Induced Obese Mice.

Obesity is associated with insulin resistance, glucose intolerance, inflammation, and altered neuronal activity in brain regions controlling metabolic functions including food intake, energy expenditure, and glucose homeostasis, such as the hypothalamus. In this study, we tested the hypothesis that inhibiting inflammation with minocycline could reduce adverse metabolic consequences associated with high-fat diet (HFD)-induced obesity in mice and sought to determine if metabolic improvements were associated with reduced hypothalamic microglia activity. Male C57Bl/6J mice were placed on 60% HFD for 12 weeks, with minocycline (40 mg/kg, p.

Acute Cannabigerol Administration Lowers Blood Pressure in Mice.

Cannabigerol is a cannabinoid compound synthesized by , which in its acid form acts as the substrate for both Δ-tetraydrocannabinol and cannabidiol formation. Given its lack of psychoactive effects, emerging research has focused on cannabigerol as a potential therapeutic for health conditions including algesia, epilepsy, anxiety, and cancer. While cannabigerol can bind to classical cannabinoid receptors, it is also an agonist at α2-adrenoreceptors (α2AR) which, when activated, inhibit presynaptic norepinephrine release.

Astrocytes play a critical role in mediating the effect of acute ethanol on central amygdala glutamatergic transmission.

The Central Amygdala (CeA) has been heavily implicated in many aspects of alcohol use disorder. Ethanol (EtOH) has been shown to modulate glutamatergic transmission in the lateral subdivision of the CeA, however, the exact mechanism of this modulation is still unclear. EtOH exposure is associated with increased pro-inflammatory cytokines in the CeA, and inhibition of neuroimmune cells (microglia and astrocytes) has previously been shown to reduce EtOH drinking in animal models.

Angiotensin-(1-7) Improves Integrated Cardiometabolic Function in Aged Mice.

Angiotensin (Ang)-(1-7) is a beneficial renin-angiotensin system (RAS) hormone that elicits protective cardiometabolic effects in young animal models of hypertension, obesity, and metabolic syndrome. The impact of Ang-(1-7) on cardiovascular and metabolic outcomes during aging, however, remains unexplored. This study tested the hypothesis that Ang-(1-7) attenuates age-related elevations in blood pressure and insulin resistance in mice.

Access schedules mediate the impact of high fat diet on ethanol intake and insulin and glucose function in mice.

Alcoholism and high fat diet (HFD)-induced obesity individually promote insulin resistance and glucose intolerance in clinical populations, increasing risk for metabolic diseases. HFD can also stimulate alcohol intake in short-term clinical studies. Unfortunately, there is currently a disconnect between animal models and the clinical findings, as animal studies typically show that HFD decreases ethanol intake while ethanol intake mitigates HFD-induced effects on insulin and glucose dysfunction.

Sex differences in metabolic effects of angiotensin-(1-7) treatment in obese mice.

Background: Angiotensin-(1-7) is a beneficial hormone of the renin-angiotensin system known to play a positive role in regulation of blood pressure and glucose homeostasis. Previous studies have shown that in high-fat diet (HFD)-induced obese male mice, circulating angiotensin-(1-7) levels are reduced and chronic restoration of this hormone reverses diet-induced insulin resistance; however, this has yet to be examined in female mice. We hypothesized angiotensin-(1-7) would improve insulin sensitivity and glucose tolerance in obese female mice, to a similar extent as previously observed in male mice.

Angiotensin-(1-7) contributes to insulin-sensitizing effects of angiotensin-converting enzyme inhibition in obese mice.

Angiotensin-converting enzyme (ACE) inhibitors reduce body weight, lower blood pressure (BP), and improve insulin sensitivity in animal models of cardiometabolic syndrome. These effects are generally attributed to reduced angiotensin (ANG) II formation; however, these therapies also increase levels of ANG-(1-7), a beneficial hormone opposing ANG II actions. We hypothesized that this ANG-(1-7) generation contributes to the insulin-sensitizing effects of ACE inhibition in obese mice.