Proopiomelanocortin Processing in the Pituitary, Central Nervous System, and Peripheral Tissues

Adiponectin, an adipose tissue-derived hormone, plays integral roles in lipid and glucose metabolism in peripheral tissues, such as the skeletal muscle, adipose tissue, and liver. Moreover, it has also been shown to have an impact on metabolic processes in the central nervous system. Astrocytes comprise the most abundant cell type in the central nervous system and actively participate in metabolic processes between blood vessels and neurons. However, the ability of adiponectin to control nutrient metabolism in astrocytes has not yet been fully elucidated. In this study, we investigated the effects of adiponectin on multiple metabolic processes in hypothalamic astrocytes. Adiponectin enhanced glucose uptake, glycolytic processes and fatty acid oxidation in cultured primary hypothalamic astrocytes. In line with these findings, we also found that adiponectin treatment effectively enhanced synthesis and release of monocarboxylates. Overall, these data suggested that adiponectin triggers catabolic processes in astrocytes, thereby enhancing nutrient availability in the hypothalamus.

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Distribution of the prion protein in sheep terminally affected with BSE following experimental oral transmission

Journal of General Virology ◽

10.1099/0022-1317-82-10-2319 ◽

2001 ◽

Vol 82 (10) ◽

pp. 2319-2326 ◽

Cited By ~ 89

Author(s):

J. D. Foster ◽

D. W. Parnham ◽

N. Hunter ◽

M. Bruce

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Experimental Infection ◽

Oral Route ◽

Similar Distribution ◽

Peripheral Tissues ◽

Oral Transmission ◽

Wide Range ◽

Direct Contrast ◽

The Central Nervous System

This study has examined the distribution of PrPSc in sheep by immunocytochemistry of tissues recovered from terminally affected animals following their experimental infection by the oral route with BSE. Despite a wide range of incubation period lengths, affected sheep showed a similar distribution of high levels of PrPSc throughout the central nervous system. PrPSc was also found in the lymphoid system, including parts of the digestive tract, and some components of the peripheral nervous system. These abundant PrPSc deposits in sheep in regions outside the central nervous system are in direct contrast with cattle infected with BSE, which show barely detectable levels of PrPSc in peripheral tissues. A number of genetically susceptible, challenged animals appear to have survived.

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Abstract 14: Central Nervous System Deletion of the Bbs1 Gene Causes Obesity and Hypertension in Mice

Hypertension ◽

10.1161/hyp.62.suppl_1.a14 ◽

2013 ◽

Vol 62 (suppl_1) ◽

Author(s):

Deng-Fu Guo ◽

Donald A Morgan ◽

Charles C Searby ◽

Darryl Y Nishmura ◽

Val C Sheffield ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Body Weight ◽

Arterial Pressure ◽

Energy Homeostasis ◽

Autosomal Recessive Disorder ◽

Conditional Knockout ◽

Peripheral Tissues ◽

Knock Out ◽

Obesity Phenotype

Bardet-Biedl syndrome (BBS) is a pleiotropic autosomal recessive disorder with several features including obesity and hypertension. Systemic knock-out mouse models lacking expression of Bbs2, Bbs4 and Bbs6 genes, and Bbs1 M390R knock-in recapitulated many of the BBS phenotypes including obesity. However, the role and contribution of different tissues to the various phenotypes associated with BBS including obesity and hypertension remains unclear. To address this, we generated a new conditional knockout mouse where exon 3 of the Bbs1 gene is floxed. Cre-mediated recombination causes a frame shift resulting in a premature stop. We assessed whether deletion of the Bbs1 gene in the central nervous system (CNS) affects body weight and arterial pressure. Breeding Bbs1 flox with nestin Cre mice created mice deficient in Bbs1 gene only in the CNS as indicated by the loss of Bbs1 gene expression (by RT-PCR) in the hypothalamus, hippocampus, cortex and brainstem, but not in peripheral tissues such as adipose tissue, liver, kidney and skeletal muscle. Importantly, Bbs1 flox /nestin Cre mice display an obesity phenotype as indicated by the increased (P<0.05) body weight (40±1 g vs. 31±1 g in controls) and fat mass measured by MRI (23±2 g vs. 9±1 g in controls) in 25 weeks old mice. We found that the obesity phenotype in Bbs1 flox /nestin Cre mice is due to both an increase (P<0.05) in food intake (4.0±0.2 g vs. 3.1±0.3 g in controls) and reduction in energy expenditure as indicated by the decreased (P<0.05) O 2 consumption (2.8±0.3 mL/100g/min vs. 3.2±0.2 mL/100g/min in controls) and heat production (8.3±0.8 kcal/kg/h vs. 9.4±0.7 kcal/kg/h in controls). These results indicate that hyperphagia and low metabolic rate explain the development of obesity in Bbs1 flox /nestin Cre mice. Finally, we assessed by radiotelemetry the consequence on arterial pressure of ablating the Bbs1 gene throughout the CNS. Interestingly, CNS deletion of the Bbs1 gene recapitulates the hypertension phenotype of BBS as indicated by the elevated mean arterial pressure in Bbs1 flox /nestin Cre (123±3 mmHg) relative to littermate controls (112±4 mmHg, P=0.02). These findings demonstrate that Bbs genes in the CNS are critical for energy homeostasis and arterial pressure regulation.

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Foreign body responses in mouse central nervous system mimic natural wound responses and alter biomaterial functions

Nature Communications ◽

10.1038/s41467-020-19906-3 ◽

2020 ◽

Vol 11 (1) ◽

Author(s):

Timothy M. OʼShea ◽

Alexander L. Wollenberg ◽

Jae H. Kim ◽

Yan Ao ◽

Timothy J. Deming ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Foreign Body ◽

Molecular Mechanisms ◽

Host Cells ◽

Peripheral Tissues ◽

Molecular Delivery ◽

Wound Responses ◽

The Central Nervous System

AbstractBiomaterials hold promise for therapeutic applications in the central nervous system (CNS). Little is known about molecular factors that determine CNS foreign body responses (FBRs) in vivo, or about how such responses influence biomaterial function. Here, we probed these factors in mice using a platform of injectable hydrogels readily modified to present interfaces with different physiochemical properties to host cells. We found that biomaterial FBRs mimic specialized multicellular CNS wound responses not present in peripheral tissues, which serve to isolate damaged neural tissue and restore barrier functions. We show that the nature and intensity of CNS FBRs are determined by definable properties that significantly influence hydrogel functions, including resorption and molecular delivery when injected into healthy brain or stroke injuries. Cationic interfaces elicit stromal cell infiltration, peripherally derived inflammation, neural damage and amyloid production. Nonionic and anionic formulations show minimal levels of these responses, which contributes to superior bioactive molecular delivery. Our results identify specific molecular mechanisms that drive FBRs in the CNS and have important implications for developing effective biomaterials for CNS applications.

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Distribution of myomodulin-like and buccalin-like immunoreactivities in the central nervous system and peripheral tissues of the mollusc,Clione limacina

The Journal of Comparative Neurology ◽

10.1002/(sici)1096-9861(19970428)381:1<41::aid-cne4>3.0.co;2-k ◽

1997 ◽

Vol 381 (1) ◽

pp. 41-52 ◽

Cited By ~ 7

Author(s):

T.P. Norekian ◽

R.A. Satterlie

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Peripheral Tissues ◽

The Central Nervous System ◽

Clione Limacina

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n-3 PUFA and obesity: from peripheral tissues to the central nervous system

British Journal Of Nutrition ◽

10.1017/s0007114518000429 ◽

2018 ◽

Vol 119 (11) ◽

pp. 1312-1323 ◽

Cited By ~ 8

Author(s):

Aline Haas de Mello ◽

Marcela Fornari Uberti ◽

Bianca Xavier de Farias ◽

Nathalia Alberti Ribas de Souza ◽

Gislaine Tezza Rezin

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Cardiac Arrhythmias ◽

The Body ◽

Low Grade ◽

Therapeutic Approaches ◽

Peripheral Tissues ◽

Inflammatory State ◽

The Central Nervous System ◽

Inflammatory Effect

AbstractThe current paradigms of prevention and treatment are unable to curb obesity rates, which indicates the need to explore alternative therapeutic approaches. Obesity leads to several damages to the body and is an important risk factor for a number of other chronic diseases. Furthermore, despite the first alterations in obesity being observed and reported in peripheral tissues, studies indicate that obesity can also cause brain damage. Obesity leads to a chronic low-grade inflammatory state, and the therapeutic manipulation of inflammation can be explored. In this context, the use of n-3 PUFA (especially in the form of fish oil, rich in EPA and DHA) may be an interesting strategy, as this substance is known by its anti-inflammatory effect and numerous benefits to the body, such as reduction of TAG, cardiac arrhythmias, blood pressure and platelet aggregation, and has shown potential to help treat obesity. Thereby, the aim of this narrative review was to summarise the literature related to n-3 PUFA use in obesity treatment. First, the review provides a brief description of the obesity pathophysiology, including alterations that occur in peripheral tissues and at the central nervous system. In the sequence, we describe what are n-3 PUFA, their sources and their general effects. Finally, we explore the main topic linking obesity and n-3 PUFA. Animal and human studies were included and alterations on the whole organism were described (peripheral tissues and brain).

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