Skin tone preferences and their influence on skin care behaviors.

Knowledge regarding skin tone preferences and their influence on skincare behaviors among people of color is limited. The objective of this study was to determine whether there is a difference between ideal and actual skin tone among people of color and whether this difference is associated with tanning and sunscreen use. This was a one-time, voluntary, anonymous, electronic survey designed in REDCap and delivered through ResearchMatch, a national electronic, recruitment tool. Eligible participants were at least 18 years old and self-identified as Black, Asian, Latinx, American Indian/Alaskan Native or Mixed Race. In total, 548 completed survey results were analyzed using SAS. Only the Latinx population was found to have a significant preference for tanner skin (p < 0.05). The Latinx population had significantly more subjects that participated in outdoor tanning than both the Black (p < 0.0001) and Asian population (p < 0.05). Latinx participants who indicated a preference for tanner skin were 2.8 times more likely to never use sunscreen than those without this preference (OR = 2.821, CI = 1.029-7.732, p < 0.05). Our findings have implications for how dermatologists screen, treat, and educate Latinx and skin of color populations.

Ventromedial hypothalamic nucleus neuronal subset regulates blood glucose independently of insulin.

To identify neurons that specifically increase blood glucose from among the diversely functioning cell types in the ventromedial hypothalamic nucleus (VMN), we studied the cholecystokinin receptor B-expressing (CCKBR-expressing) VMN targets of glucose-elevating parabrachial nucleus neurons. Activation of these VMNCCKBR neurons increased blood glucose. Furthermore, although silencing the broader VMN decreased energy expenditure and promoted weight gain without altering blood glucose levels, silencing VMNCCKBR neurons decreased hIepatic glucose production, insulin-independently decreasing blood glucose without altering energy balance. Silencing VMNCCKBR neurons also impaired the counterregulatory response to insulin-induced hypoglycemia and glucoprivation and replicated hypoglycemia-associated autonomic failure. Hence, VMNCCKBR cells represent a specialized subset of VMN cells that function to elevate glucose. These cells not only mediate the allostatic response to hypoglycemia but also modulate the homeostatic setpoint for blood glucose in an insulin-independent manner, consistent with a role for the brain in the insulin-independent control of glucose homeostasis.

A leptin-regulated circuit controls glucose mobilization during noxious stimuli.

Adipocytes secrete the hormone leptin to signal the sufficiency of energy stores. Reductions in circulating leptin concentrations reflect a negative energy balance, which augments sympathetic nervous system (SNS) activation in response to metabolically demanding emergencies. This process ensures adequate glucose mobilization despite low energy stores. We report that leptin receptor-expressing neurons (LepRb neurons) in the periaqueductal gray (PAG), the largest population of LepRb neurons in the brain stem, mediate this process. Application of noxious stimuli, which often signal the need to mobilize glucose to support an appropriate response, activated PAG LepRb neurons, which project to and activate parabrachial nucleus (PBN) neurons that control SNS activation and glucose mobilization. Furthermore, activating PAG LepRb neurons increased SNS activity and blood glucose concentrations, while ablating LepRb in PAG neurons augmented glucose mobilization in response to noxious stimuli. Thus, decreased leptin action on PAG LepRb neurons augments the autonomic response to noxious stimuli, ensuring sufficient glucose mobilization during periods of acute demand in the face of diminished energy stores.