Disease relevance of Sat

• Alveolar and total lung SP-A and Sat PC were higher relative to body weight and surface area on d 1 than at all other ages [1].
• In the in vitro ischemia study, SSAT activity was evaluated in primary cortical neuronal cultures at 6-24 h re-oxygenation intervals following oxygen-glucose deprivation for 1 h, and the results from this group show that the enzyme activity increased by about 62% (P<0.05) at 24 h re-oxygenation [2].
• In the present study, SSAT activity was evaluated in the rat CNS, following transient focal cerebral ischemia and reperfusion [2].

High impact information on Sat

• Cardiac triglyceride content was increased in the Sat and Unsat groups compared with NC (P < 0.05); however, ceramide content was higher in the Sat group compared with the Unsat group (2.9 +/- 0.2 vs. 1.4 +/- 0.2 nmol/g; P < 0.05), whereas the NC group was intermediate (2.3 +/- 0.3 nmol/g) [3].
• Both high-fat diets increased the myocardial mRNA expression of the PPAR-regulated genes encoding uncoupling protein-3 and pyruvate dehydrogenase kinase-4, but only the Sat diet upregulated medium-chain acyl-CoA dehydrogenase [3].
• The number of apoptotic myocytes, assessed by terminal deoxynucleotide transferase-mediated dUTP nick-end labeling staining, was higher in the Sat group compared with the Unsat group (0.28 +/- 0.05 vs. 0.17 +/- 0.04 apoptotic cells/1,000 nuclei; P < 0.04) and was positively correlated to ceramide content (P < 0.02) [3].
• This study assessed cardiac function, expression of PPAR-regulated genes, and cardiomyocyte apoptosis in rats after 8 wk on either a low-fat diet [normal chow control (NC); 10% fat calories] or high-fat diets composed mainly of either saturated (Sat) or unsaturated fatty acids (Unsat) (60% fat calories) (n = 10/group) [3].
• We asked how the quantities of the surfactant components surfactant protein A (SP-A) and saturated phosphatidylcholine (Sat PC) recovered by alveolar wash changed with age in relationship to morphologic measurements of alveolar surface area in rats [1].

Anatomical context of Sat

• However, the peak increase of SSAT labelling was precocious in resistant neurons (such as those of ventromedial striatum and dentate gyrus granular layer) and delayed or very limited in vulnerable neurons (such as those of CA1 pyramidal layer and dorsolateral striatum) [4].
• DXR was found to induce significant ECG alterations (Qat and Sat prolongation) and typical morphologic lesions in the left ventricle [5].

Associations of Sat with chemical compounds

• This study suggests that the increased SSAT activity may contribute to the increase in putrescine during the post-ischemic period [2].
• Spermidine/Spermine N(1)-acetyl transferase (SSAT) is the key enzyme responsible for interconversion of spermine and spermidine to spermidine and putrescine respectively [2].
• The polyamine putrescine might be formed via a degradation (catalyzed by spermidine/spermine N1-acetyltransferase, SSAT) of the higher polyamines spermidine and spermine to putrescine [6].
• Pilocarpine, a drug that activates the muscarinic receptors and thereby enhances the phosphoinositide turnover, had no effect on either the polyamine concentrations or on the SSAT activity [6].
• The beta-adrenoceptor agonist isoprenaline, which is an activator of cAMP formation, increased the putrescine concentration and stimulated the SSAT activity [6].

Analytical, diagnostic and therapeutic context of Sat

• Animals were sacrificed at 3-24 h reperfusion following the MCA occlusion and SSAT activity was assayed in cortex and striatum [2].

References