Cover Story Current Issue

Despite intensive drug development efforts and public health initiatives, obesity is increasing in incidence and predicted to affect over 50% of all adults worldwide by 2035. Being chronically overweight increases the risk of serious disease co-morbidities that, in turn, increase mortality and healthcare costs. Behavioral approaches to combat obesity, such as diet and exercise, rarely produce lasting weight loss commonly due to compensatory hyperphagia and hypometabolism. These limitations have stimulated interest in pharmacotherapies that target gut-derived peptide hormones involved in the regulation of energy homeostasis, such as PYY, GIP, CCK, and GLP-1. These peptides are secreted by different enteroendocrine cells distributed throughout the intestine in response to food intake, subsequently enhancing satiation signaling and ultimately promotes meal termination. However, a major challenge of FDA-approved and experimental weight-loss medications that target GI-derived satiation signals is the frequent occurrence of nausea and vomiting.

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Current Issue

Oxytocin neurons in the paraventricular and supraoptic hypothalamic nuclei bidirectionally modulate food intake

Jessica J. Rea, Clarissa M. Liu, Anna M.R. Hayes, Rita Ohan, ... Scott E. Kanoski

Oxytocin neurons in the paraventricular and supraoptic hypothalamic nuclei bidirectionally modulate food intake

 

Objectives

Oxytocin (OT) is a neuropeptide produced in the paraventricular (PVH) and supraoptic (SON) nuclei of the hypothalamus. Either peripheral or central OT administration reduces food intake through reductions in meal size. However, pharmacological approaches do not differentiate whether OT's influence on food intake is mediated by OT neurons located in the PVH vs. the SON. Here we address this gap using both gain- and loss-of-function approaches targeting OT neurons.

Methods

OT neuron-specific designer receptors exclusively activated by designer drugs (DREADDs) were targeted in either the PVH or SON in rats, thus allowing for evaluation of caloric intake following selective activation of OT neurons separately in each nucleus. To examine the physiological role of distinct OT neuron populations in eating behavior, a viral-mediated approach was used to silence synaptic transmission of OT neurons separately in either the PVH or SON.

Results

DREADDs-mediated excitation of PVH OT neurons reduced consumption of standard chow via reductions in meal size. On the contrary, SON OT neuron activation had the opposite effect by increasing standard chow consumption. Consistent with these opposing outcomes, activation of PVH and SON OT neurons simultaneously had minimal effects on food intake. Additional results from chronic loss-of-function experiments reveal that PVH OT neuron silencing significantly increased consumption of a high fat and high sugar diet by increasing meal size whereas SON OT neuron silencing reduced chow consumption by decreasing meal size.

Conclusions

Collectively these findings suggest that PVH and SON OT neurons differentially modulate food intake by either reducing or increasing caloric consumption, respectively.

 

Articles in Press

Oxytocin neurons in the paraventricular and supraoptic hypothalamic nuclei bidirectionally modulate food intake

Jessica J. Rea, Clarissa M. Liu, Anna M.R. Hayes, Rita Ohan, ... Scott E. Kanoski

Oxytocin neurons in the paraventricular and supraoptic hypothalamic nuclei bidirectionally modulate food intake

 

Objectives

Oxytocin (OT) is a neuropeptide produced in the paraventricular (PVH) and supraoptic (SON) nuclei of the hypothalamus. Either peripheral or central OT administration reduces food intake through reductions in meal size. However, pharmacological approaches do not differentiate whether OT's influence on food intake is mediated by OT neurons located in the PVH vs. the SON. Here we address this gap using both gain- and loss-of-function approaches targeting OT neurons.

Methods

OT neuron-specific designer receptors exclusively activated by designer drugs (DREADDs) were targeted in either the PVH or SON in rats, thus allowing for evaluation of caloric intake following selective activation of OT neurons separately in each nucleus. To examine the physiological role of distinct OT neuron populations in eating behavior, a viral-mediated approach was used to silence synaptic transmission of OT neurons separately in either the PVH or SON.

Results

DREADDs-mediated excitation of PVH OT neurons reduced consumption of standard chow via reductions in meal size. On the contrary, SON OT neuron activation had the opposite effect by increasing standard chow consumption. Consistent with these opposing outcomes, activation of PVH and SON OT neurons simultaneously had minimal effects on food intake. Additional results from chronic loss-of-function experiments reveal that PVH OT neuron silencing significantly increased consumption of a high fat and high sugar diet by increasing meal size whereas SON OT neuron silencing reduced chow consumption by decreasing meal size.

Conclusions

Collectively these findings suggest that PVH and SON OT neurons differentially modulate food intake by either reducing or increasing caloric consumption, respectively.

 

SAVE THE DATE!

13th
Helmholtz Diabetes Conference 
Munich, 21-23. Sep 2026                                                                                                                             

2024 impact factor: 6.6

You are what you eat

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