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os. Glycine intake decreases plasma free fatty acids, adipose cell size, and blood pressure in sucrose-fed rats. Am J Physiol Regul Integr Comp Physiol 287: R1387-R1393, 2004. First published August 26, 2004 doi:10.1152/ajpregu.00159.2004The study investigated the mechanism by which glycine protects against increased circulating nonesterified fatty acids (NEFA), fat cell size, intra-abdominal fat accumulation, and blood pressure (BP) induced in male Wistar rats by sucrose ingestion. The addition of 1% glycine to the drinking water containing 30% sucrose, for 4 wk, markedly reduced high BP in sucrose-fed rats (SFR) (122.3 Ϯ 5.6 vs. 147.6 Ϯ 5.4 mmHg in SFR without glycine, P Ͻ 0.001). Decreases in plasma triglyceride (TG) levels (0.9 Ϯ 0.3 vs. 1.4 Ϯ 0.3 mM, P Ͻ 0.001), intra-abdominal fat (6.8 Ϯ 2.16 vs. 14.8 Ϯ 4.0 g, P Ͻ 0.01), and adipose cell size were observed in SFR treated with glycine compared with SFR without treatment. Total NEFA concentration in the plasma of SFR was significantly decreased by glycine intake (0.64 Ϯ 0.08 vs. 1.11 Ϯ 0.09 mM in SFR without glycine, P Ͻ 0.001). In control animals, glycine decreased glucose, TGs, and total NEFA but without reaching significance. In SFR treated with glycine, mitochondrial respiration, as an indicator of the rate of fat oxidation, showed an increase in the state IV oxidation rate of the ␤-oxidation substrates octanoic acid and palmitoyl carnitine. This suggests an enhancement of hepatic fatty acid metabolism, i.e., in their transport, activation, or ␤-oxidation. These findings imply that the protection by glycine against elevated BP might be attributed to its effect in increasing fatty acid oxidation, reducing intra-abdominal fat accumulation and circulating NEFA, which have been proposed as links between obesity and hypertension. obesity; mitochondrial oxygen uptake; fatty acid oxidation OBESITY is a significant human health problem; its incidence is reaching epidemic proportions in many Western countries (2, 31). Obesity with fat accumulation predominantly in the abdominal cavity is more frequently associated with disorders of glucose and lipid metabolism than is subcutaneous fat obesity (6, 17). It is well known that increased intra-abdominal fat accumulation is also associated with elevated circulating nonesterified fatty acids (NEFA) (33), resulting from the increased lipolytic activity in adipose tissue. High levels of circulating NEFA have been assumed to be a possible link between intra-abdominal fat accumulation and elevated blood pressure (BP) (9,34,46,49).Several factors are known to be involved in the development of intra-abdominal adiposity in both humans and animals, including genetic and environmental factors, such as excessive fat or carbohydrate intake and lack of physical exercise (8, 44). Thus several animal models of obesity have been developed to investigate the mechanism by which obesity induces hypertension, hyperinsulinemia, and insulin resistance.In our laboratory, we developed an animal model of intraabdominal fat accumulation, indu...

It has not been definitely established whether elevated circulating triglyceride-rich lipoproteins constitute an independent risk factor for hypertension, atherosclerosis, myocardial infarction, and coronary heart disease. To investigate some aspects of the physiopathology of this lipid metabolism abnormality, a model of experimental hypertriglyceridemia and hypertension in rats was studied. The animals received commercially refined sugar (30%) in their drinking water during a period of 12 to 17 weeks. Monthly measurements of blood pressure and serum triglycerides were taken during and at the end of the treatment period; the levels of glucose and insulin were also determined. The blood, the aorta, and mesenteric artery were removed. Age- and weight-matched controls were used. The reactivity of the isolated vessels to norepinephrine and acetylcholine and the effect of control and hypertriglyceridemic serum on the same preparations were investigated. In hypertriglyceridemic rats, the response to acetylcholine in the tissues was reduced compared to the control arteries; the hypertriglyceridemic serum elicited contractions that were greater than those induced by control serum. The impaired response of hypertriglyceridemic tissue to the vasodilator and the effect of the hypertriglyceridemic serum on artery contraction suggest that the overall dyslipidemia could contribute to a chronic increase in vascular tone and, consequently, to hypertension.

This paper deals with the so-called Stanley conjecture, which asks whether they are non-isomorphic trees with the same symmetric function generalization of the chromatic polynomial. By establishing a correspondence between caterpillars trees and integer compositions, we prove that caterpillars in a large class (we call trees in this class proper) have the same symmetric chromatic function generalization of the chromatic polynomial if and only if they are isomorphic.