scholarly journals The SNPs of Melanocortin 4 Receptor (MC4R) Associated with Body Weight in Beagle Dogs

2014 ◽  
Vol 63 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Ruixia Zeng ◽  
YiBo Zhang ◽  
Peng Du
1992 ◽  
Vol 29 (3) ◽  
pp. 230-238 ◽  
Author(s):  
J. E. Burkhardt ◽  
M. A. Hill ◽  
J. J. Turek ◽  
W. W. Carlton

The ultrastructural features of quinolone-induced arthropathy were studied in' the humeral and femoral heads of nine skeletally immature Beagle dogs (3 months old) that were dosed orally with difloxacin at 300 mg/kg body weight and euthanatized 24, 36, or 48 hours later in groups of three. Three age-matched dogs were given a placebo and euthanatized after 48 hours. Mitochondria in chondrocytes had significantly greater cross-sectional areas ( P < 0.05) in electron micrographs from dogs euthanatized after 48 hours of treatment than did those in other groups. There was also a significantly greater percentage of chondrocytes with swollen mitochondria in treated dogs than in the controls ( P < 0.05). These changes preceded the necrosis observed in some chondrocytes in the dogs of the 48-hour group. Disruption of extracellular matrix was first observed in the pericellular matrix of necrotic chondrocytes, indicating that this change was secondary to the changes in chondrocytes. Fissures within cartilages apparently resulted from the loss of the normal association of proteoglycans with collagen fibrils.


eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Giuseppe D'Agostino ◽  
David J Lyons ◽  
Claudia Cristiano ◽  
Luke K Burke ◽  
Joseph C Madara ◽  
...  

The nucleus of the solitary tract (NTS) is a key gateway for meal-related signals entering the brain from the periphery. However, the chemical mediators crucial to this process have not been fully elucidated. We reveal that a subset of NTS neurons containing cholecystokinin (CCKNTS) is responsive to nutritional state and that their activation reduces appetite and body weight in mice. Cell-specific anterograde tracing revealed that CCKNTS neurons provide a distinctive innervation of the paraventricular nucleus of the hypothalamus (PVH), with fibers and varicosities in close apposition to a subset of melanocortin-4 receptor (MC4RPVH) cells, which are also responsive to CCK. Optogenetic activation of CCKNTS axon terminals within the PVH reveal the satiating function of CCKNTS neurons to be mediated by a CCKNTS→PVH pathway that also encodes positive valence. These data identify the functional significance of CCKNTS neurons and reveal a sufficient and discrete NTS to hypothalamus circuit controlling appetite.


1972 ◽  
Vol 27 (02) ◽  
pp. 220-227
Author(s):  
D McDonald ◽  
Blanche Jackson ◽  
H. B Boudreaux ◽  
R. B Myers

SummaryPeroral administration of choline in relatively high dosage (300 or 600 mg choline dihydrogen citrate per 17-20 lb body weight, 4 times daily) caused no significant change in serum antiplasmin activity of either normal or factor VIII-deficient beagle dogs. Also, no alteration in antiplasmin level was found to be associated with the hemophilic state.Canine serum antiplasmins are stable at low temperatures. Like human antiplasmins, they appear to have two major components which differ conspicuously in stability at 60° C.Other data presented in this paper show that crude plasmin readily obtained from human serum euglobulins provides an enzyme preparation suitable for screening antiplasmin levels of sera by the caseinolytic method.


Author(s):  
Jesse Z. Dong ◽  
Daniel B. DeOliveira ◽  
Heather A. Halem ◽  
John E. Taylor ◽  
Pierre Roubert ◽  
...  

1981 ◽  
Vol 18 (6) ◽  
pp. 769-777 ◽  
Author(s):  
D. M. Hoover ◽  
W. W. Carlton ◽  
C. K. Henrikson

Three adult Beagle dogs given pyridoxine hydrochloride orally at a dose of 150 mg/kg body weight/day for about 100 days developed ataxia and had spastic, dysmetric leg movements. Ultrastructural alterations in the dorsal funiculus of the spinal cord were degeneration and loss of axons and myelin, and secondary changes of the myelin sheaths. Possible pathogenic mechanisms of pyridoxine neurotoxicity are discussed.


2009 ◽  
Vol 38 (1) ◽  
pp. 98-111 ◽  
Author(s):  
Sender Lkhagvadorj ◽  
Long Qu ◽  
Weiguo Cai ◽  
Oliver P. Couture ◽  
C. Richard Barb ◽  
...  

Transcriptional profiling coupled with blood metabolite analyses were used to identify porcine genes and pathways that respond to a fasting treatment or to a D298N missense mutation in the melanocortin-4 receptor (MC4R) gene. Gilts (12 homozygous for D298 and 12 homozygous for N298) were either fed ad libitum or fasted for 3 days. Fasting decreased body weight, backfat, and serum urea concentration and increased serum nonesterified fatty acid. In response to fasting, 7,029 genes in fat and 1,831 genes in liver were differentially expressed (DE). MC4R genotype did not significantly affect gene expression, body weight, backfat depth, or any measured serum metabolite concentration. Pathway analyses of fasting-induced DE genes indicated that lipid and steroid synthesis was downregulated in both liver and fat. Fasting increased expression of genes involved in glucose sparing pathways, such as oxidation of amino acids and fatty acids in liver, and in extracellular matrix pathways, such as cell adhesion and adherens junction in fat. Additionally, we identified DE transcription factors (TF) that regulate many DE genes. This confirms the involvement of TF, such as PPARG, SREBF1, and CEBPA, which are known to regulate the fasting response, and implicates additional TF, such as ESR1. Interestingly, ESR1 controls several fasting induced genes in fat that are involved in cell matrix morphogenesis. Our findings indicate a transcriptional response to fasting in two key metabolic tissues of pigs, which was corroborated by changes in blood metabolites, and the involvement of novel putative transcriptional regulators in the immediate adaptive response to fasting.


1981 ◽  
Vol 18 (6) ◽  
pp. 745-756 ◽  
Author(s):  
D. M. Hoover ◽  
W. W. Carlton

The clinical and clinicopathologic effects of excess oral pyridoxine hydrochloride (150 mg/kg body weight/day) and clioquinol (200 mg/kg body weight/day) alone and in combination were evaluated in adult Beagle dogs over an experimental period of approximately 100 days. Anorexia and loss of body weight occurred in the first weeks of the trial period in each treatment group, but was most severe in dogs given both compounds. Dogs in each treatment group (10 of 10 pyridoxine-treated dogs, 6 of 13 clioquinol-treated dogs and 12 of 13 pyridoxine plus clioquinol-treated dogs) developed neurologic disease, manifested principally by ataxia. Pyridoxine-treated dogs had proprioceptive loss involving both fore- and hindquarters, characterized by stiff, spastic, dysmetric leg movements. In clioquinol-treated dogs, dysmetric leg movements were accompanied by failure to support body weight in the hindquarters, but similar forelimb involvement occurred in severely affected dogs. The neurologic disease in dogs given both compounds varied; signs in some dogs resembled those of affected dogs of the pyridoxine-treated group, and in others, those in the clioquinol-treated group. Erythrocyte counts, hemoglobin concentrations and packed cell volumes were reduced in dogs in each treatment group and were lowest in dogs given both compounds. Plasma protein was mildly reduced in dogs given pyridoxine or pyridoxine plus clioquinol. Few or no differences were present in the leukocyte counts, blood urea nitrogen concentrations, in activities of serum alanine aminotransferase and aspartate aminotransferase, and in concentrations of sodium, chloride or potassium in treated dogs as compared to control dogs.


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