Study of Serum Leptin in Cafeteria-Diet-Overfed Rats

Schepper, J. De; Bock, S. De; Smitz, Johan; Louis, Olivia; Hooghe‐Peters, Elisabeth L.; Vandenplas, Yvan

doi:10.1159/000023289

Cited by 12 publications

(6 citation statements)

References 18 publications

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“…In the present study, only 4 weeks on a hyperlipidic diet, both continuously and alternated with a chow diet, caused an enhancement in adiposity that was accompanied by an increase in serum leptin concentration, which shows that short periods of hyperlipidic diets can promote obesity. In previous studies, several obese animal models have also developed elevated circulating leptin levels [15,40]. …”

Section: Discussionmentioning

confidence: 99%

“…Previous experiments have shown that rats fed a high-fat diet had an increased fat mass percentage even when the energy intake was not elevated [15,16]. Likewise, we previously demonstrated that the continuous intake of a hyperlipidic palatable diet and the alternation of a high-fat intake with periods of chow intake for 8 weeks caused obesity and affected the lipid metabolism of rats in a similar way, although the energy intake remained unchanged (KJ) [17].…”

Section: Introductionmentioning

confidence: 99%

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A palatable hyperlipidic diet causes obesity and affects brain glucose metabolism in rats

et al. 2011

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BackgroundWe have previously shown that either the continuous intake of a palatable hyperlipidic diet (H) or the alternation of chow (C) and an H diet (CH regimen) induced obesity in rats. Here, we investigated whether the time of the start and duration of these feeding regimens are relevant and whether they affect brain glucose metabolism.MethodsMale Wistar rats received C, H, or CH diets during various periods of their life spans: days 30-60, days 30-90, or days 60-90. Experiments were performed the 60th or the 90th day of life. Rats were killed by decapitation. The glucose, insulin, leptin plasma concentration, and lipid content of the carcasses were determined. The brain was sliced and incubated with or without insulin for the analysis of glucose uptake, oxidation, and the conversion of [1-14C]-glucose to lipids.ResultsThe relative carcass lipid content increased in all of the H and CH groups, and the H30-60 and H30-90 groups had the highest levels. Groups H30-60, H30-90, CH30-60, and CH30-90 exhibited a higher serum glucose level. Serum leptin increased in all H groups and in the CH60-90 and CH30-90 groups. Serum insulin was elevated in the H30-60, H60-90, CH60-90, CH30-90 groups. Basal brain glucose consumption and hypothalamic insulin receptor density were lower only in the CH30-60 group. The rate of brain lipogenesis was increased in the H30-90 and CH30-90 groups.ConclusionThese findings indicate that both H and CH diet regimens increased body adiposity independent treatment and the age at which treatment was started, whereas these diets caused hyperglycemia and affected brain metabolism when started at an early age.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A palatable hyperlipidic diet causes obesity and affects brain glucose metabolism in rats

et al. 2011

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“…However, a number of reports showed that serum leptin levels did not change significantly during the estrus cycle in rats [28, 29, 30]. On the other hand, Bennet et al [31]reported that serum leptin levels tended to increase during proestrus in rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of Estrogen on Serum Leptin Levels and Leptin mRNA Expression in Adipose Tissue in Rats

et al. 2001

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Objective: In this study, we examined changes in serum leptin levels during the estrus cycle and the role of estrogen in these changes. Methods: We measured serum leptin levels during normal estrus cycles in intact rats and estradiol-17β (E₂)-induced artificial estrus cycles in ovariectomized rats. Results: Serum leptin levels increased 1.6-fold from 4.2 ± 0.2 ng/ml during diestrus stage 2 to 6.7 ± 0.9 ng/ml during proestrus stage during the 4-day estrus cycle. During the E₂-induced estrus cycle, serum leptin levels increased 2.3-fold from 2.3 ± 0.1 ng/ml at estrus to 5.4 ± 1.2 ng/ml at proestrus. E₂ also increased serum leptin concentrations and leptin mRNA expression in adipose tissue of immature rats. Discussion: These findings suggest that increased serum leptin induced by estrogen during proestrus may trigger the preovulatory release of luteinizing hormone. Furthermore, our findings indicate that estrogen has a positive effect on leptin production in adipose tissue.

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“…As a result of excessive calorie intake for example, leptin resistance has been proposed to provoke diet-induced obesity in animals and humans (3). Most studies have shown that high-fat diets can both increase the ob gene expression in adipose tissue and augment circulating leptin levels (4)(5)(6). However, controversy exists since high-fat diets also have been associated with a suppression of plasma leptin levels (7).…”

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confidence: 99%

Impact of Dietary FA and Energy Restriction on Plasma Leptin and ob Gene Expression in Mice

Gregersen

Thomsen

Jeppesen

et al. 2003

Lipids

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The aim of the present study was to elucidate whether the qualitative composition of dietary fat influences plasma leptin and adipose tissue ob gene expression differentially. Two high-fat diets and a diet rich in carbohydrate were each administered both ad libitum and with a 25% energy restriction. The high-fat diets contained 58 energy percent as either monounsaturated FA (MUFA) or saturated FA (SAFA), whereas the carbohydrate-rich diet (CH) contained 7 energy percent as fat. We aimed at obtaining the same final weight for the animals in the ad libitum group as in the energy-restricted groups. This goal was reached at the same time (days 22-24) for all groups except for the ad libitum animals fed on saturated fat (day 36). The plasma leptin concentrations on ad libitum CH and MUFA diets did not differ significantly (24.3 +/- 2.1 and 34.7 +/- 6.7 ng/mL, respectively) whereas the saturated fat diet caused a lower concentration (13.9 +/- 1.9 ng/mL; P < 0.05). Interestingly, no differences in plasma leptin levels between groups were seen in the energy-restricted groups (mean 8.0 +/- 1.0 ng/mL). The type of diet did not alter the ob gene expression in intraabdominal white adipose tissue; however, a lower expression level was found in the energy-restricted groups. The percentage of body fat in the three ad libitum fed groups did not differ (23 +/- 1%). Thus, short-term administration of a diet rich in SAFA suppresses circulating leptin levels without altering the adipose tissue ob gene expression. This indicates that saturated fat may alter protein handling by adipose tissue or the whole body clearance of leptin.

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Study of Serum Leptin in Cafeteria-Diet-Overfed Rats

Cited by 12 publications

References 18 publications

A palatable hyperlipidic diet causes obesity and affects brain glucose metabolism in rats

A palatable hyperlipidic diet causes obesity and affects brain glucose metabolism in rats

Effects of Estrogen on Serum Leptin Levels and Leptin mRNA Expression in Adipose Tissue in Rats

Impact of Dietary FA and Energy Restriction on Plasma Leptin and ob Gene Expression in Mice

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