Effect of oral oleoyl-estrone treatment on plasma lipoproteins and tissue lipase activities of Zucker lean and obese female rats

Blay, Mayte; Peinado-Onsurbe, Júlia; Grasa, Mar; Díaz-Silva, M; Fernández-López, José Antonio; Remesar, Xavier; Alemany, M

doi:10.1038/sj.ijo.0801985

Cited by 30 publications

(36 citation statements)

References 39 publications

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“…11 This is accomplished essentially by facilitating the use of fatty acids by the muscle and other peripheral tissues, 13 decreasing the oxidation of glucose and increasing its storage as glycogen, 10 and, at the same time, decreasing insulin resistance. 11,26 Under OE, glucose levels are maintained in spite of a marked decrease of insulin.…”

Section: Discussionmentioning

confidence: 99%

“…The characteristic effect of OE decreasing circulating cholesterol, 10,12 also observed here, is largely independent of the mobilisation of lipids (controls' levels practically did not change with dietary restriction), but is directly correlated with an enhanced lipoprotein metabolism. 12,13 The marked effects of OE on leptin 10,12 hint at deeply altered adipocyte signalling pathways, the uncharacteristic decreases of adiponectin elicited by OE attest that there is no direct or easy explanation of the mobilising effects of OE. Adiponectin and leptin levels usually show reversed patterns, leptin levels being high in the obese, 30 which usually show low adiponectin concentrations.…”

Section: Discussionmentioning

confidence: 99%

“…10 Lipid mobilisation, however, does not massively increase circulating lipids, since lipid oxidation is also increased as shown by the lowering of the respiratory quotient, 5 and marked decrease in cholesterol levels 12 coupled with enhanced muscle lipoprotein lipase activity. 13 Human obesity has been traditionally treated with hypocaloric diets, since it is assumed that a decrease in energy intake must compel the body to mobilise its fat stores to cope with the energy imbalance; however, dieting tends to decrease energy expenditure, 14 which makes much harder to significantly affect the mass of stored fat. The considerable difficulty in shedding off fat through dieting is compounded by the recovery of energy stores when food availability is restablished.…”

Section: Introductionmentioning

confidence: 99%

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Combined effects of oral oleoyl-estrone and limited food intake on body composition of young overweight male rats

2006

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Objective: The combined effects of limited food intake and OE treatment have been analysed in order to determine whether hypocaloric diets enhance the slimming effects of OE on mature overweight male rats. Two levels of dietary limitation at 50 and 25% of a standard intake were established, roughly corresponding to the human LCDs and VLCDs. Design: Wistar male rats (6 weeks old) were made overweight by a cafeteria diet. After transition to standard diet, they were subjected to food restriction: down to 50 or 25% with respect to the transition period. Half the animals were given daily oral gavages of 10 nmol/g oleoyl-estrone (OE), and the rest received only the vehicle during 10 days. Measurements: Changes in weight and body composition: water, lipid, protein or gross energy were determined by comparing the final pool size with that of day 0, calculated from the initial body weight and the composition of untreated rats. Energy and nitrogen balances were estimated. Plasma levels of metabolites and hormones were also measured. Results: OE induced changes in body composition similar to those elicited by a 50% reduction in food, with massive loss of lipid and energy. OE-treated rats ate less than the controls, but additional effects on body composition on reduced diet were minimal. OE improved metabolic homoeostasis: better maintained glycaemia, lower cholesterol and shallower hormonal changes, but at the expense of slightly increased protein mobilisation. Conclusions: The data presented suggest that no advantages are accomplished by combining OE treatment and hypocaloric diets compared with OE alone, at least under the experimental conditions tested, since the effects were not additive. Despite OE affecting food intake, mechanisms other than that are deemed responsible for the mobilisation of body fat, since intake alone cannot explain the effects on body weight, nor the metabolic and hormonal changes in OE-treated rats. It is concluded that the combination of food restriction and OE may result in unwanted increased protein mobilisation with no synergy between both slimming treatments.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Combined effects of oral oleoyl-estrone and limited food intake on body composition of young overweight male rats

2006

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“…1 Oral gavages result in a dose-dependent loss of weight, 2 mostly due to the mobilisation of body lipids. This active utilisation of lipid reserves is carried out essentially by decreasing the lipid stores in white adipose tissue, 1 and the increased muscle utilisation of lipids 3 that result in a marked decrease of the respiratory quotient, 1 sparing body protein in a context in which food intake was decreased and energy expenditure maintained. 4 Chronic oleoyl-estrone treatment also induces a decrease in insulin levels and insulin resistance, with maintenance of plasma glucose and liver glycogen.…”

Section: Introductionmentioning

confidence: 99%

“…Nevertheless, the effects of oleoyl-estrone on food intake were already observable after 2 h of the oral administration of the hormone. 8 Oleoyl-estrone decreases circulating cholesterol, especially in the HDL fraction, 3 but does not alter the body cholesterol pool to a significant extent; 7 thus, any changes in plasma cholesterol dynamics may reflect modifications in lipoprotein turnover in addition to eventual changes in the rates of synthesis or excretion of cholesterol. Since the mobilisation of cholesterol and its transport via the blood is one of the most marked effects of oleoyl-estrone on lipid metabolism, we studied the turnover rate of cholesterol in rat plasma shortly after a single dose of oral oleoyl-estrone, when massive lipid mobilisation had not yet been fully established.…”

Section: Introductionmentioning

confidence: 99%

Short-term oral oleoyl-estrone treatment increases plasma cholesterol turnover in the rat

et al. 2005

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OBJECTIVE: Oral treatment with oleoyl-estrone induces the loss of body fat and improvement of insulin resistance. Since cholesterol levels are deeply affected by oleoyl-estrone, we investigated here whether short-term treatment affected cholesterol turnover and overall metabolite changes. DESIGN: Wistar female rats received a single oral dose of 10 mmol/kg oleoyl-estrone in 0.2 ml of sunflower oil. Groups of animals were killed at timed intervals and blood samples were taken. In a second experiment series, rats had implanted carotid and jugular cannulas and were given a single gavage of oleoyl-estrone. These rats were used for the measurement of the cholesterol turnover rate. MEASUREMENTS: Body weight change and food intake: Glucose, total and HDL-cholesterol, triacylglycerols, 3-hydroxybutyrate, nonesterified fatty acids, insulin, HOMA score in the rats of the first series. Cholesterol: Cholesterol pool changes and cholesterol turnover rates in the rats of the second series. RESULTS: OE induced early effects, decreasing food intake, cholesterol and HDL-cholesterol levels, and increasing insulin sensitivity (HOMA score). OE also increased cholesteryl-ester turnover, and decreased circulating total cholesterol, especially esterified cholesterol pools. CONCLUSIONS: The role of early changes in insulin sensitivity induced by oral OE cannot explain per se the deep changes in cholesterol handling, essentially a consequence of accelerated lipoprotein turnover. However, the increase in cholesteryl-ester turnover observed with OE treatment may be, at least in part, a consequence of the decrease in insulin resistance. The compounded effect of increased insulin sensitivity and accelerated lipoprotein turnover may help explain the early and marked hypocholesterolaemic effects of OE.

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Oleoyl‐Estrone

Remesar

Fernández-López

Alemany

2011

Medicinal Research Reviews

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Oleoyl-estrone (OE) is a powerful slimming agent that is also present in plasma and adipose tissue, where it is synthesized. It acts through the formation of a derivative W. OE effects (and W levels) are proportional to the dose. OE reduces food intake but maintains energy expenditure (thermogenesis). The energy gap is fulfilled with adipose tissue fat, sparing body protein and maintaining glycemia (and glycogen) with lower insulin and leptin levels. OE (in fact W) acts through specific receptors, different from those of estrogen. OE increases cholesterol catabolism, reducing hypercholesterolemia in obese rats. The main metabolic effect on adipose tissue is lowering of lipid synthesis, maintaining unchanged the intracellular lipolytic processes; the imbalance favors the progressive loss of fat, which is largely used by the muscle. OE administration induces additive effects with other antiobesity agents, such as β(3)-adrenergic agonists, forcing a massive loss of lipid. Corticosteroids markedly limit OE action by altering the liver control of lipogenesis. OE also inhibits the action of 17β-hydroxysteroid dehydrogenase, decreasing the synthesis of β-estradiol and testosterone. Discontinuous treatment allows for maximal efficacy both in rats and humans. OE has the advantage that the loss of fat is maintained and does not require additional dietary limitations.

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Effect of oral oleoyl-estrone treatment on plasma lipoproteins and tissue lipase activities of Zucker lean and obese female rats

Cited by 30 publications

References 39 publications

Combined effects of oral oleoyl-estrone and limited food intake on body composition of young overweight male rats

Combined effects of oral oleoyl-estrone and limited food intake on body composition of young overweight male rats

Short-term oral oleoyl-estrone treatment increases plasma cholesterol turnover in the rat

Oleoyl‐Estrone

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