scholarly journals Role of pituitary adenylate cyclase-activating polypeptide in energy expenditure including the thermogenic response

2020 ◽  
Author(s):  
◽  
Daemon Lee Cline
Keyword(s):  
Energy Expenditure ◽  
Adenylate Cyclase ◽  
Pituitary Adenylate Cyclase ◽  
Thermogenic Response

scholarly journals Emerging Role of PACAP as a New Potential Therapeutic Target in Major Diabetes Complications

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Rubina Marzagalli ◽  
Soraya Scuderi ◽  
Filippo Drago ◽  
James A. Waschek ◽  
Alessandro Castorina
Keyword(s):  
Life Expectancy ◽  
Adenylate Cyclase ◽  
Diabetes Complications ◽  
Increase Life Expectancy ◽  
Potential Therapeutic Target ◽  
Future Directions ◽  
Major Complications ◽  
Secondary Damage ◽  
Pituitary Adenylate Cyclase

Enduring diabetes increases the probability of developing secondary damage to numerous systems, and these complications represent a cause of morbidity and mortality. Establishing the causes of diabetes remains the key step to eradicate the disease, but prevention as well as finding therapies to ameliorate some of the major diabetic complications is an equally important step to increase life expectancy and quality for the millions of individuals already affected by the disease or who are likely to develop it before cures become routinely available. In this review, we will firstly summarize some of the major complications of diabetes, including endothelial and pancreatic islets dysfunction, retinopathy, and nephropathy, and then discuss the emerging roles exerted by the neuropeptide pituitary adenylate cyclase activating polypeptide (PACAP) to counteract these ranges of pathologies that are precipitated by the prolonged hyperglycemic state. Finally, we will describe the main signalling routes activated by the peptide and propose possible future directions to focus on developing more effective peptide-based therapies to treat the major complications associated with longstanding diabetes.

scholarly journals SAT-LB107 Insulin Sensing by Astrocytes Is Critical for Normal Thermogenesis and Body Temperature Regulation

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jennifer Wootton Hill ◽  
Iyad H Manaserh
Keyword(s):  
Body Temperature ◽  
Energy Expenditure ◽  
Insulin Signaling ◽  
Insulin Receptors ◽  
Normal Body Temperature ◽  
Metabolic Dysregulation ◽  
Brown Adipose ◽  
Novel Target ◽  
Thermogenic Response

Abstract The important role of astrocytes in the central control of energy balance and glucose homeostasis has only recently been recognized. Changes in thermoregulation can lead to metabolic dysregulation, but the role of astrocytes in this process is not yet clear. Therefore, we generated mice congenitally lacking insulin receptors (IR) in astrocytes (IRKOGFAP mice) to investigate the involvement of astrocyte insulin signaling. IRKOGFAP mice displayed a significant decrease in energy expenditure and a striking decrease in basal and fasting body temperature. When exposed to cold, however, they were able to mount a thermogenic response. Brown adipose tissue in IRKOGFAP mice exhibited increased adipocyte size, more apoptosis, loss of innervation, and decreased βAR3 expression levels. These findings identify a novel role for astrocyte insulin signaling in the development of normal body temperature control and sympathetic activation of BAT. Targeting insulin signaling in astrocytes has the potential to serve as a novel target for increasing energy expenditure.

Pituitary adenylate cyclase-activating peptide stimulates cyclic AMP accumulation in UMR 106 osteoblast-like cells

1996 ◽  
Vol 149 (2) ◽  
pp. 287-295 ◽  
Author(s):  
C S Kovacs ◽  
C L Chik ◽  
B Li ◽  
E Karpinski ◽  
A K Ho
Keyword(s):  
Adenylate Cyclase ◽  
Bone Cells ◽  
Tumor Cell Line ◽  
Camp Accumulation ◽  
Kinase C ◽  
Cyclic Amp Accumulation ◽  
Pituitary Adenylate Cyclase ◽  
And Function ◽  
Umr 106

Abstract Pituitary adenylate cyclase-activating peptide (PACAP) and vasoactive intestinal peptide (VIP) share 68% homology and function as neurotransmitters or neuroendocrine factors. Although VIP immunoreactivity has been detected in bone cells, the presence of PACAP or PACAP receptors in bone has not been determined. In this study, we investigated the role of PACAP and VIP in regulating cAMP accumulation in the UMR 106 osteoblast-like tumor cell line. PACAP 27 (10−9 to 3 × 10−7 m), PACAP 38 (10−9 to 3 × 10−7 m) and VIP (10−8 to 10−6 m) stimulated cAMP accumulation up to eightfold. PACAP 27 was slightly more potent than PACAP 38, and both were tenfold more potent than VIP. Both PACAP- and VIP-stimulated cAMP accumulation were potentiated by 4β-phorbol 12-myristate 13-acetate, an activator of protein kinase C. Two PACAP antagonists, PACAP 6–27 (3 × 10−6 m) and PACAP 6–38 (3 × 10−6 m), blocked PACAP- and VIP-stimulated cAMP accumulation. Two VIP antagonists ([Lys1,Pro2,5,Arg3,4,Tyr6]-VIP, and 4 Cl-d-Phe6,Leu17]-VIP) did not reduce the PACAP-or VIP-stimulated cAMP accumulation. Pretreatment with PACAP 27, PACAP 38 or VIP equally blocked PACAP- and VIP-stimulated cAMP accumulation. These results suggest that PACAP is a more potent stimulator of cAMP accumulation than VIP in UMR 106 cells. PACAP and VIP may share a role in the paracrine or neuroendocrine regulation of bone metabolism. Journal of Endocrinology (1996) 149, 287–295

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