scholarly journals Low Carbohydrate/High-Fat Diet Attenuates Cardiac Hypertrophy, Remodeling, and Altered Gene Expression in Hypertension

Hypertension ◽  
2006 ◽  
Vol 48 (6) ◽  
pp. 1116-1123 ◽  
Author(s):  
Isidore C. Okere ◽  
Martin E. Young ◽  
Tracy A. McElfresh ◽  
David J. Chess ◽  
Victor G. Sharov ◽  
...  
PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0192606 ◽  
Author(s):  
Madeline Rose Keleher ◽  
Rabab Zaidi ◽  
Shyam Shah ◽  
M. Elsa Oakley ◽  
Cassondra Pavlatos ◽  
...  

2002 ◽  
Vol 362 (1) ◽  
pp. 113-118 ◽  
Author(s):  
Sophie TURBAN ◽  
Isabelle HAINAULT ◽  
Johan TRUCCOLO ◽  
Jocelyne ANDRE ◽  
Pascal FERRE ◽  
...  

In the obese state, enlarged adipose cells display an altered gene-expression profile and metabolic capacity. The aim of this study was to gain insight into their secretory function, by assessing two secreted proteins, leptin and angiotensinogen, in adipose cells of obese (fa/fa) Zucker rats. A marked and co-ordinate increase in leptin mRNA, gene transcription and promoter activity was observed in obese compared with lean (Fa/fa) rat adipose cells, and this resulted in increased leptin release in culture. Two sets of observations suggest that this effect is due to the fa mutation. First, adipose-cell leptin release was higher in heterozygous (Fa/fa) than in homozygous (Fa/Fa) lean rats. Second, leptin release was not enhanced in enlarged adipose cells of FalFa rats fed a high-fat diet for 15 days. At variance with leptin, angiotensinogen production was not significantly increased in the obese cells. Dexamethasone stimulated both leptin and angiotensinogen release in lean and obese rat adipose cells. The magnitude of leptin stimulation was higher in fa/fa than in Fa/fa rats, whereas angiotensinogen release was increased to the same extent in both genotypes. These observations suggest that leptin production is specifically enhanced in enlarged adipose cells of obese Zucker rats and that cell hypertrophy is not the sole determinant of this feature. Increased leptin production might be related to disruption of leptin signalling by the fa mutation.


Author(s):  
W. K. Jones ◽  
J. Robbins

Two myosin heavy chains (MyHC) are expressed in the mammalian heart and are differentially regulated during development. In the mouse, the α-MyHC is expressed constitutively in the atrium. At birth, the β-MyHC is downregulated and replaced by the α-MyHC, which is the sole cardiac MyHC isoform in the adult heart. We have employed transgenic and gene-targeting methodologies to study the regulation of cardiac MyHC gene expression and the functional and developmental consequences of altered α-MyHC expression in the mouse.We previously characterized an α-MyHC promoter capable of driving tissue-specific and developmentally correct expression of a CAT (chloramphenicol acetyltransferase) marker in the mouse. Tissue surveys detected a small amount of CAT activity in the lung (Fig. 1a). The results of in situ hybridization analyses indicated that the pattern of CAT transcript in the adult heart (Fig. 1b, top panel) is the same as that of α-MyHC (Fig. 1b, lower panel). The α-MyHC gene is expressed in a layer of cardiac muscle (pulmonary myocardium) associated with the pulmonary veins (Fig. 1c). These studies extend our understanding of α-MyHC expression and delimit a third cardiac compartment.


Endoscopy ◽  
2004 ◽  
Vol 36 (05) ◽  
Author(s):  
K Collins ◽  
GA Doherty ◽  
MR Sweeney ◽  
SM Byrne ◽  
AA Aftab ◽  
...  

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