Responses of lean and obese Zucker rats to centrally administered leptin

Wang, Tianlun; Hartzell, Diane L.; Flatt, William P.; Martin, Roy J.; Baile, Clifton A.

doi:10.1016/s0031-9384(98)00173-5

Cited by 40 publications

(27 citation statements)

References 24 publications

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“…[10][11][12] Leptin resistance is also found in the most common cases of human obesity, for unknown reasons although considered to be multi-factorial and polygenic in nature. [13][14][15] In conclusion, this is the first evidence for an animal model that reproduces changes in body weight that occur in obese humans after bariatric surgery with gastric banding.…”

Section: Discussionmentioning

confidence: 99%

A Rat Model of Restrictive Bariatric Surgery with Gastric Banding

Monteiro¹,

Monteiro²,

Águas³

et al. 2006

obes surg

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Background: Gastric banding is a well established weight reduction operation that is effective in the treatment of severe obesity. Its metabolic and endocrine mechanisms of action, however, remain unclear. The aim of this study was to establish a rat model of gastric banding that would replicate the procedure performed in human obese patients.Methods: Male Wistar rats were submitted either to gastric banding (n=5) or sham gastric banding (n=4), and were followed for 21 days. Detailed description on how to perform gastric banding in rats are herein described.Results: The Wistar rats submitted to gastric banding showed a decrease in weight gain and food intake when compared to sham-operated rats.The cumulative weight gain during the 21 days after the surgical procedure was 143 ± 2.58 g for the gastric banded rats and 162 ± 2.48 g for the sham-operated animals (P=0.001). The cumulative food intake was 329 ± 0.53 g for the gastric banded rats and 380 ± 15.22 g for the sham-operated animals, also statistically significant (P=0.025).Conclusion: A rat model to study gastric banding is described. This model can now be used for experimental investigation of biochemical and molecular mechanisms of weight loss resulting from this type of surgery.

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Section: Discussionmentioning

confidence: 99%

A Rat Model of Restrictive Bariatric Surgery with Gastric Banding

Monteiro¹,

Monteiro²,

Águas³

et al. 2006

obes surg

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“…A higher set point of the cerebral adipostat present in obese individuals may be the result of a relative or absolute insensitivity to leptin. Daily injections of leptin decreased appetite and body weight in both ob/ob mice and wild-type mice and increased energy expenditure in lean new-born Zucker rats (6)(7)(8). Leptin deficiency caused genetic obesity in ob/ob mice as well as in a recently described family kindred (9).…”

Section: Obesity Is Associated With a Decreased Leptin Transport Acromentioning

confidence: 97%

Obesity is associated with a decreased leptin transport across the blood-brain barrier in rats.

et al. 2000

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Leptin exerts important effects on the regulation of food intake and energy expenditure by acting in the brain. Leptin is secreted by adipocytes into the bloodstream and must gain access to specific regions in the brain involved in regulating energy balance. Its action is mediated by interaction with a receptor that is mainly expressed in the hypothalamus but is also present in other cerebral areas. To reach these target areas, leptin most likely needs to cross the blood-brain barrier (BBB). In this study, we compared the permeability of leptin at the BBB in homozygous lean (FA/FA), high-fat diet-induced (HFD) obese rats (FA/FA rats on a highfat diet), and genetically obese fa/fa Zucker rats by quantifying the permeability coefficient surface area (PS) product after correction for the residual plasma volume (V p ) occupied by leptin in the vessel bed of different brain regions. The intravenous bolus injection technique was used in the cannulated brachial vein and artery using leptin radioiodinated with 2 isotopes of iodine ( 125 I and 131 I) to separately determine the PS and V p values. The PS for leptin at the BBB in lean FA/FA rats ranged from 11.0 ± 1.6 at the cortex to 14.8 ± 1.4 ؋ 10 -6 ml · g -1 · ml -1 at the posterior hypothalamus. The PS for leptin in HFD obese FA/FA and obese fa/fa rats ranged from 3.0-to 4.0-fold lower than in lean FA/FA rats. The V p values were not significantly different among the 3 groups studied. SDS-PAGE analysis of the radioiodinated leptin after 60 min of uptake revealed intact protein in the 8 different brain regions. Plasma leptin levels were significantly higher in both obese rat groups compared with those in lean FA/FA rats. Leptin levels in cerebrospinal fluid were not significantly different among the 3 groups of rats. These findings strongly suggest that the leptin receptor (OB-R) in the BBB can be easily saturated. Saturation of the BBB OB-R in obese individuals would explain the defect in leptin transport into the brain described in this study.

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“…We also investigated leptin variations in our experiment because ghrelin and leptin are closely and reciprocally regulated (Barazzoni et al 2003, Kalra et al 2003 and despite the mutation in the leptin receptor gene (Chua et al 1996, Iida et al 1996, the obese Zucker rat is not totally leptin unresponsive. It shows a blunted response after leptin injection (AlBarazanji et al 1997, Wang et al 1998 presenting therefore a leptin resistance that is also present in obese subjects (Considine et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Dietary modulation of ghrelin and leptin and gorging behavior after weight loss in the obese Zucker rat

Beck¹,

Richy²

2009

Journal of Endocrinology

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In this study, we measured ghrelin and leptin in obese Zucker rats after weight loss induced by calorie restriction using either a low-fat (LF) or high-energy palatable (HEPa) diet. After weight loss, the animals were refed lab chow and offered one hour-palatable test meals on the second and fifteenth days of refeeding. Both LF and HEPa rats lost 10% of their initial body weight (P!0 . 0001). Plasma ghrelin increased with calorie restriction in both groups (P!0 . 002) with a tendency to a higher increase in the HEPa group while plasma leptin decreased only in the LF group (P!0 . 01). Both groups ate the same quantity of chow during refeeding and both groups gorged on palatable diet during test meals at a very high constant intensity in HEPa rats. After one week of refeeding, ghrelin levels remained elevated in HEPa rats (C33 . 2%; P!0 . 001) while returning to baseline in LF rats. Plasma leptin remained low in LF rats. We conclude that weight loss on a palatable diet is possible if total energy intake is controlled. After stopping restriction, when a palatable diet is available, observed gorging might be dependent on specific ghrelin and leptin changes.

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Responses of lean and obese Zucker rats to centrally administered leptin

Cited by 40 publications

References 24 publications

A Rat Model of Restrictive Bariatric Surgery with Gastric Banding

A Rat Model of Restrictive Bariatric Surgery with Gastric Banding

Obesity is associated with a decreased leptin transport across the blood-brain barrier in rats.

Dietary modulation of ghrelin and leptin and gorging behavior after weight loss in the obese Zucker rat

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