Justin McFarland is a familiar face to Nashville viewers, but his story extends beyond the anchor desk at FOX 17 News. From his roots in Music City to his dedication to health awareness, McFarland's journey is one of continuous growth and commitment.
From Local Roots to News Anchor
Justin's connection to Nashville runs deep. Moving to the city at the young age of 11, he witnessed its transformation firsthand, recalling a time "before the Batman Building." He attended F. H. Jenkins Preparatory and Madison Academy, establishing a foundation in the community he now serves as a journalist.
His career began as a sports reporter for the Tennessee Tribune, showcasing his early passion for storytelling. He further honed his skills at various radio stations and continues to host a talk radio show that airs in Huntsville, Alabama, demonstrating his ongoing commitment to broadcasting.
Justin's path to the anchor desk wasn't a direct one. From 2009 to 2014, he served as a morning reporter for FOX 17 News. He then spent several years as the Morning and Midday News Anchor at WAAY-TV in Huntsville, Alabama, gaining valuable experience before returning to Nashville. Prior to his promotion to the anchor desk, Justin also served as the FOX 17 Steer Clear Traffic Anchor.
Award-Winning Journalism and Athletic Prowess
Justin's dedication to his craft has been recognized with four Emmy Award nominations and one win. This recognition speaks to his talent and commitment to delivering high-quality journalism.
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Beyond his broadcasting career, Justin McFarland is also a notable athlete. As a key player on the Bloomsburg Huskies football team, he demonstrated intensity and skill.
The Link Between Obesity and Cardiovascular Health
The American Heart Association (AHA) has identified obesity as a major obstacle in improving cardiovascular health, including hypertension. While various interventions such as drugs, exercise, diets, and surgeries can lead to weight loss, maintaining a reduced weight in the long term remains a challenge. The AHA's 2020 Impact Goal aimed to improve cardiovascular health by 20% and reduce deaths from cardiovascular diseases and stroke by 20%. While progress was made in areas like reduced smoking and increased physical activity, increases in high blood pressure and body mass index offset these gains.
It is estimated that a significant percentage of adult Americans are overweight or obese, and obesity trends continue to rise. Obesity is linked to increased mortality and is a major risk factor for cardiovascular and metabolic diseases. Hypertension and obesity elevate the risk of stroke, myocardial infarction, heart failure, and renal failure, while obesity also promotes type 2 diabetes, another significant cardiovascular risk factor.
The Body's Defense of Increased Body Mass
Sustained obesity leads to changes in energy homeostasis, causing the body to defend an increased body mass. Clinical studies have demonstrated that after weight loss, individuals exhibit robust resting metabolic rate (RMR) adaptation, meaning the body adjusts to burn fewer calories. This adaptation, which can equate to a 5% change in energy expenditure, highlights the difficulty in maintaining weight loss. Given that adult obesity in the USA is estimated to result from a chronic energy surplus of only approximately 7 kcal/day, the pathophysiological significance of a 5% RMR adaptation is profound.
The Renin-Angiotensin System and Resting Metabolic Rate
The renin-angiotensin system (RAS) plays a role in cardiovascular physiology and metabolic physiology. It influences RMR through multiple mechanisms. Within adipose tissue, Ang-II acts via its type 2 receptor (AT2R) to modulate adipocyte differentiation, reducing the thermogenic response to autonomic stimuli. This results in reduced RMR responses. The RAS also controls RMR through actions in the brain, specifically within the hypothalamic arcuate nucleus (ARC). Studies have investigated the interaction between leptin and Ang-II in the control of cardiovascular and thermogenic autonomic functions.
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Conditional genetic deletion of AT1R from cells expressing the leptin receptor (LEPR) or Agouti-related peptide (AgRP) impairs normal autonomic and RMR responses to stimuli like leptin, DOCA-salt, and high-fat diets. Similarly, conditional deletion of AT1R from neurons expressing Sim1 interferes with integrated control of energy expenditure. The effect of transgenic activation of the brain RAS to stimulate RMR is not additive to the effects of leptin, suggesting an overlap of mechanisms.
The hypothalamic melanocortin system mediates many of leptin's functions. Mice deficient for the melanocortin type 4 receptor (MC4R) exhibit normal blood pressure responses but a complete loss of RMR responses to acute ICV Ang-II injection. Mice with conditional deletion of AT1R from LEPR- or AgRP-expressing neurons exhibit increased expression of genes producing neurotransmitters generated by AgRP neurons. These mice also exhibited blunted RMR responses to acute injection of an MC4R agonist, supporting the concept that AT1R action on AgRP neurons acts to suppress AgRP-mediated inhibition of postsynaptic MC4R signaling for RMR control. Leptin requires AT1R on specific neurons to stimulate RMR, but stimulation of the brain RAS via DOCA-salt does not require leptin signaling to do the same.
AgRP Neuron Subtypes and Resting Metabolic Rate Control
Multiple subtypes of Agouti-related peptide (AgRP) neurons exist within the arcuate nucleus of the hypothalamus (ARC). These subtypes can be differentiated based on their expression of receptors like AT1R and AT2R. The Type 1 subtype is inhibited by AT1R signaling, which reduces inhibitory AgRP neurotransmission to postsynaptic targets. This disinhibits MC4R in relevant cells of the medial preoptic area (MPO), increasing excitatory glutamatergic signaling to the dorsomedial hypothalamus (DMH), and ultimately increasing thermogenic sympathetic nervous activity (SNA) and resting metabolic rate (RMR). Distinct Type 1 AgRP neurons project to the PVN and appear to utilize Neuropeptide-Y (NPY) transmission to postsynaptic Y1R receptors to influence cardiovascular SNA and blood pressure.
Single-cell RNA sequencing methods have revealed distinct clusters of AgRP neurons. One cluster, termed [Sst-3, medium], expresses somatostatin (SST) and detectable levels of AT1R, angiotensinogen (AGT/Agt), the pro-renin receptor (PRR/Atp6ap2), and ACE. Another cluster, [GABA-14], does not express AT1R but expresses AGT, PRR, ACE, the MasR, and the Ang-II type 4 receptor. Similarly, other studies have identified AgRP neuron clusters with high and low expression of SST. These findings suggest that SST expression differentiates some subtypes of AgRP neurons.
Electrophysiological studies have distinguished three unique subtypes of AgRP neurons based on their electrochemical responses to Ang-II: Type 0 (non-responsive), Type 1 (AT1R-inhibited), and Type 2 (AT2R-stimulated). Type 1 AgRP neurons are uniquely involved in controlling energy expenditure, while Type 0 / Type 2 AgRP neurons mediate feeding control. Type 1 AgRP neurons project to the supraoptic nucleus (SON), bed nucleus of the stria terminalis (BNST), paraventricular nucleus (PVN), and medial preoptic nucleus (MPO). The preoptic area (POA), including the MPO, is a primary site for integrative control of thermogenesis, energy expenditure, and thermoregulatory behaviors. Only two neuron clusters within the MPO robustly express MC4R: [E8] and [E12]. Both clusters are glutamatergic and do not express typical markers of warm-sensitive neurons.
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Arcuate Nucleus and Cardiovascular Functions
The ARC also plays a role in controlling cardiovascular functions. Microinjection of Ang-II into the ARC increases arterial pressure through an AT1R-dependent cascade. ARC efferent pathways to the PVN and DMH are involved in this pressor response and are mediated, at least partially, through the NPY receptor Y1 (Y1R).