Effect of sucrose addition to drinking water, that induces hypertension in the rats, on liver microsomal Δ9 and Δ5-desaturase activities

Hafidi, Mohammed El; Cuéllar, Adela; Ramı́rez, Jorge; Baños, Guadalupe

doi:10.1016/s0955-2863(01)00154-1

Cited by 60 publications

(45 citation statements)

References 37 publications

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“…The lowering effect of glycine on the concentration of monounsaturated fatty acids, such as oleic acid, may be related to the lowering effect on BP in the SFRG. The increased palmitoleic and oleic acid concentrations in plasma and liver from SFR reflect an increase of the ⌬9-desaturase activity as described previously (18). The sucrose diet reduced the amount of linoleic acid, a precursor of arachidonic acid.…”

Section: Discussionsupporting

confidence: 75%

“…Fasting plasma glucose levels were not significantly different between the groups. Fasting plasma TGs and insulin were significantly higher in SFR (P Ͻ 0.001 and P Ͻ 0.001, respectively) than in control animals, as described previously (18). Glycine treatment of SFR significantly reduced insulin and TGs to the normal levels found in control animals (Table 1).…”

Section: Energy Intake and Liquid And Food Consumptionsupporting

confidence: 83%

“…The obtained lipid residue was dissolved in 1 ml methanol, and NEFA were esterified to their corresponding methyl esters as described by Tserng et al (50) and modified by McClelland et al (35). The concentration and composition of NEFA were evaluated by gas-liquid chromatography as described previously (18).…”

Section: Methodsmentioning

confidence: 99%

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Glycine intake decreases plasma free fatty acids, adipose cell size, and blood pressure in sucrose-fed rats

Hafidi¹,

Pérez²,

Zamora³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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105

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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...

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Section: Discussionsupporting

confidence: 75%

Section: Energy Intake and Liquid And Food Consumptionsupporting

confidence: 83%

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Glycine intake decreases plasma free fatty acids, adipose cell size, and blood pressure in sucrose-fed rats

Hafidi¹,

Pérez²,

Zamora³

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

Self Cite

105

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“…The method used in this work has the advantage of limiting the time of lipid extract exposure to autooxidation. The concentration and composition of FFA methyl esters were evaluated by gas liquid chromatography, as described previously (17).…”

Section: Methodsmentioning

confidence: 99%

“…Because the primary function of UCP2 is to mediate proton leak, the overexpression of UCP2 in fatty liver may compromise ATP biosynthesis (8). In a model of abdominal obesity induced by a high-sucrose diet, the increased FFA level in both plasma and the liver (17)(18)(19) suggests mitochondrial dysfunction accompanied by high reactive oxygen species (ROS) generation and oxidative stress in the liver. Generation of ROS in response to a hyperlipidemic environment may also contribute to the maintenance of a normal or altered redox status of the liver in this model of abdominal obesity.…”

mentioning

confidence: 99%

High-sucrose diet increases ROS generation, FFA accumulation, UCP2 level, and proton leak in liver mitochondria

Ruiz-Ramírez

Chávez-Salgado

Peñeda-Flores

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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M. High-sucrose diet increases ROS generation, FFA accumulation, UCP2 level, and proton leak in liver mitochondria. Am J Physiol Endocrinol Metab 301: E1198 -E1207, 2011. First published September 13, 2011 doi:10.1152/ajpendo.00631.2010.-Obesity, a risk factor for insulin resistance, contributes to the development of type 2 diabetes and cardiovascular diseases. The relationship between increased levels of free fatty acids in the liver mitochondria, mitochondrial function, and ROS generation in rat model of obesity induced by a high-sucrose diet was not sufficiently established. We determined how the bioenergetic functions and ROS generation of the mitochondria respond to a hyperlipidemic environment. Mitochondria from sucrose-fed rats generated H2O2 at a higher rate than the control mitochondria. Adding fatty acid-free bovine serum albumin to mitochondria from sucrose-fed rats significantly reduced the rate of H2O2 generation. In contrast, adding exogenous oleic or linoleic acid exacerbated the rate of H2O2 generation in both sucrose-fed and control mitochondria, and the mitochondria from sucrose-fed rats were more sensitive than the control mitochondria. The increased rate of H2O2 generation in sucrose-fed mitochondria corresponded to decreased levels of reduced GSH and vitamin E and increased levels of Cu/Zn-SOD in the intermembrane space. There was no difference between the levels of lipid peroxidation and protein carbonylation in the two types of mitochondria. In addition to the normal activity of Mn-SOD, GPX and catalase detected an increased activity of complex II, and upregulation of UCP2 was observed in mitochondria from sucrose-fed rats, all of which may accelerate respiration rates and reduce generation of ROS. In turn, these effects may protect the mitochondria of sucrose-fed rats from oxidative stress and preserve their function and integrity. However, in whole liver these adaptive mechanisms of the mitochondria were inefficient at counteracting redox imbalances and inhibiting oxidative stress outside of the mitochondria. reactive oxygen species; free fatty acid; metabolic syndrome; mitochondrial function; oxidative stress; uncoupling protein 2 ABDOMINAL OBESITY AND HIGH LEVELS of circulating free fatty acids (FFAs) have been indicated as primary contributors to acquired insulin resistance and hypertension because they induce oxidative stress that affects insulin signaling and nitric oxide availability (30, 11). Insulin resistance leads to continuous lipolysis within adipocytes, releasing FFAs into the local circulation, where they are transported into the liver. In the liver, FFAs can be incorporated into triglycerides that accumulate and lead to nonalcoholic fatty liver disease, the primary hepatic complication of obesity (13, 57). Oxidative stress and mitochondrial dysfunction have been shown to play a critical role in the initiation and progression of fatty liver to the more serious condition of nonalcoholic steatohepatitis in obesity models (15,21,38). Several studies using an animal model of fa...

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Early endocrine and molecular changes in metabolic syndrome models

et al. 2011

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SummaryThe twenty-first century arrived in the middle of a global epidemic of metabolic syndrome (MS) and type 2 diabetes mellitus (DM2). It is generally accepted that an excess of nutrients linked to a low physical activity triggers the problem. However, the molecular features that interact to develop the MS are not clear. In an effort to understand and control them, they have been extensively studied, but this goal has not been achieved yet. Nonhuman animal models have been used to explore diet and genetic factors in which experimental conditions are controlled. For example, only one factor in the diet, such as fats or carbohydrates can be modified to better understand a single change that would be impossible in humans. Most of the studies have been done in rodents. However, it is difficult to directly compare them, because experiments are different in more than one variable; genetic strains, amount, and the type of fat used in the diet and sex. Thus, the only possible criteria of comparison are the relevance of the observed changes. We review different animal models and add some original observations on short-term changes in metabolism and beta cells in our own model of adult Wistar rats that are not especially prone to get fat or develop DM2, treated with 20% sucrose in drinking water. One early change observed in pancreatic beta cells is the increase in GLUT2 expression that is located to the membrane of the cells. This change could partially explain the presence of insulin hypersecretion and hyperinsulinemia in these rats. Understanding early changes that lead to MS and in time to pancreatic islet exhaustion is an important biomedical problem that may contribute to learn how to prevent or even reverse MS, before developing DM2.

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Effect of sucrose addition to drinking water, that induces hypertension in the rats, on liver microsomal Δ9 and Δ5-desaturase activities

Cited by 60 publications

References 37 publications

Glycine intake decreases plasma free fatty acids, adipose cell size, and blood pressure in sucrose-fed rats

Glycine intake decreases plasma free fatty acids, adipose cell size, and blood pressure in sucrose-fed rats

High-sucrose diet increases ROS generation, FFA accumulation, UCP2 level, and proton leak in liver mitochondria

Early endocrine and molecular changes in metabolic syndrome models

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