Direct and indirect effects of liraglutide on hypothalamic POMC and NPY/AgRP neurons – Implications for energy balance and glucose control

He, Zhenyan; Gao, Yong; Lieu, Linh; Afrin, Sadia; Cao, Jianhong; Michael, Natalie J.; Dong, Yanbin; Sun, Jia; Guo, Hongbo; Williams, Kevin W.

doi:10.1016/j.molmet.2019.07.008

Cited by 83 publications

(116 citation statements)

References 86 publications

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“…This is similar to obscure alteration of Npy, Agrp, and Pomc mRNA expression levels after administration of liraglutide [15]. Unaltered expression of these neuropeptides is considered to be effects of GLP-1 that are not directly related to NPY/AgRP and POMC neurons [18].…”

Section: Discussionmentioning

confidence: 96%

Anagliptin suppresses diet-induced obesity through enhancing leptin sensitivity and ameliorating hyperphagia in high-fat high-sucrose diet fed mice

2020

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Obesity is a major risk factors for type 2 diabetes, and weight loss is beneficial to diabetic patients who are obese or overweight. Dipeptidyl peptidase-4 (DPP-4) inhibitors are anti-diabetic drugs. Although it has been known that the effect of most of the DPP-4 inhibitors on body weight is neutral, several studies suggested that some DPP-4 inhibitors suppressed body weight. Nonetheless, the mechanisms underlying DPP-4 inhibitor-induced weight loss are not fully understood. In this study, the mice fed high-fat high sucrose diet (HFHSD) containing a DPP4 inhibitor, anagliptin, showed reduced food intake and body weight compared to the mice fed non-treated HFHSD, but oxygen consumption and respiratory exchange ratio (RER) were not altered. Sequential administration of leptin suppressed food intake and body weight more apparently in anagliptin treated HFHSD fed mice than non-treated HFHSD fed mice. Oxygen consumption and RER were comparable between anagliptin treated and non-treated mice after leptin administration. The number of phospho STAT3 expressed cells in the arcuate nucleus after leptin administration was increased in anagliptin treated mice compared to non-treated mice. These data suggested that anagliptin ameliorated leptin resistance induced by HFHSD and thereby decreased food intake and body weight. These effects of anagliptin could be beneficial to the treatment of obese diabetic patients.

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Section: Discussionmentioning

confidence: 96%

Anagliptin suppresses diet-induced obesity through enhancing leptin sensitivity and ameliorating hyperphagia in high-fat high-sucrose diet fed mice

2020

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“…In particular, leptin, serotonin (via serotonin 2c receptors – 5-HT 2c R), adiponectin, and glucagon-like peptide 1 (GLP-1) serve to activate, while insulin inhibits POMC neurons via their cognate receptors [ 5 , 48 , 52 , 82 , 98 , 99 , 102 , 103 , 108 , 109 , 161 , 163 , 174 , 180 , 181 ]. Conversely, leptin, serotonin (via serotonin 1b receptors - 5-HT 1b R), adiponectin, insulin, and GLP-1 inhibit NPY/AgRP cells [ 5 , 13 , 48 , 98 , 99 , 103 , 111 , 127 , 163 , 190 ]. While leptin, serotonin, adiponectin, and insulin directly inhibit NPY/AgRP neurons, GLP-1 indirectly inhibits NPY/AgRP neurons via GABAergic synaptic connectivity [ 98 , 163 ].…”

Section: The Arcuate Nucleus: Pomc and Npy/agrp Neuronsmentioning

confidence: 99%

“…Conversely, leptin, serotonin (via serotonin 1b receptors - 5-HT 1b R), adiponectin, insulin, and GLP-1 inhibit NPY/AgRP cells [ 5 , 13 , 48 , 98 , 99 , 103 , 111 , 127 , 163 , 190 ]. While leptin, serotonin, adiponectin, and insulin directly inhibit NPY/AgRP neurons, GLP-1 indirectly inhibits NPY/AgRP neurons via GABAergic synaptic connectivity [ 98 , 163 ]. Similarly, ghrelin directly excites NPY/AgRP neurons while indirectly inhibiting POMC neurons [ 44 , 53 , 111 , 126 , 190 ].…”

Section: The Arcuate Nucleus: Pomc and Npy/agrp Neuronsmentioning

confidence: 99%

“…3 ) [ 51 , 52 , 82 , 99 , 101 , 108 , 109 , 111 , 127 , 160 , 163 , 173 , 174 , 180 , 195 , 197 , 198 ]. For example, acute leptin receptor activity in ARH POMC neurons colocalizes with adiponectin and GLP-1 receptor (GLP-1r) activity [ 98 , 180 ]. Additional work suggests that the activity of neurotensin synergizes with GLP-1r activity in POMC neurons [ 160 ].…”

Section: Metabolic Signals and Cell-type Specificity Of Hypothalamic mentioning

confidence: 99%

“…2 and Fig. 3 ) [ 12 , 16 , 17 , 34 , 82 , 98 , 108 , 111 , 127 , 160 , 163 , 180 , 189 , 203 – 205 ].…”

Section: Metabolic Signals and Cell-type Specificity Of Hypothalamic unclassified

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Dysfunction in neurophysiological systems that regulate food intake and metabolism are at least partly responsible for obesity and related comorbidities. An important component of this process is the hypothalamic melanocortin system, where an imbalance can result in severe obesity and deficits in glucose metabolism. Exercise offers many health benefits related to cardiovascular improvements, hunger control, and blood glucose homeostasis. However, the molecular mechanism underlying the exercise-induced improvements to the melanocortin system remain undefined. Here, we review the role of the melanocortin system to sense hormonal, nutrient, and neuronal signals of energy status. This information is then relayed onto secondary neurons in order to regulate physiological parameters, which promote proper energy and glucose balance. We also provide an overview on the effects of physical exercise to induce biophysical changes in the melanocortin circuit which may regulate food intake, glucose metabolism and improve overall metabolic health.

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Direct and indirect effects of liraglutide on hypothalamic POMC and NPY/AgRP neurons – Implications for energy balance and glucose control

Cited by 83 publications

References 86 publications

Anagliptin suppresses diet-induced obesity through enhancing leptin sensitivity and ameliorating hyperphagia in high-fat high-sucrose diet fed mice

Anagliptin suppresses diet-induced obesity through enhancing leptin sensitivity and ameliorating hyperphagia in high-fat high-sucrose diet fed mice

Effects of metabolic state on the regulation of melanocortin circuits

The impact of obesity‐related neuroinflammation on postpartum depression: A narrative review

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