Sensory responses, dietary-induced obesity and biochemical values in Sprague-Dawley rats

Grinker, Joel A.; Block, Walter D.

doi:10.1016/0361-9230(91)90155-d

Cited by 7 publications

(6 citation statements)

References 14 publications

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“…Metabolically, they may be predisposed to develop DIO because of a decreased capacity for fatty acid oxidation (3) secondary to a decreased percentage of type I skeletal muscle fibers (20). Contrary to the current studies, Grinker and Block (5) found that rats with an increased sucrose (but not fat) preference gained more weight on a high fat diet. But Sclafani has pointed out (22), dietary content can be a major determinant of the development of DIO.…”

Section: Discussioncontrasting

confidence: 99%

“…It is now clear that rats from the same strain can differ widely in their propensity to develop DIO on HE diets. This is true of both Sprague-Dawley (1,5,10,12,17,22) and Wistar strains (3.20). These rats often do not differ phenotypically with regard to body weight or energy intake on a diet low in fat and sucrose such as Purina rat chow (12).…”

Section: Discussionmentioning

confidence: 93%

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Sympathetic Activity, Age, Sucrose Preference, and Diet‐Induced Obesity

Levin

1993

Obesity Research

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Only half the adult male Sprague-Dawley rats which are placed on a diet relatively high in calories, fat, and sucrose (HE diet) develop diet-induced obesity (DIO). The rest are diet-resistant (DR). Some chow-fed rats prone to develop DIO on an HE diet have greater initial food intake of this diet and all have greater glucose-induced plasma norepinephrine (NE) increases than DR-prone rats. Here we looked for a relationship of sucrose preference or 24-hour urinary catecholamine excretion as possible phenotypic markers of the DIO- and DR-prone states before HE diet exposure as a function of age. When begun on an HE diet at 3 months of age, DIO-prone rats gained 30% more weight over 3 months than DR-prone rats and had 35% heavier retroperitoneal fat pads. While still on chow, sucrose preferences were similar, but 24 hour urine NE levels were 29% higher in DIO- than in DR-prone rats. The slope of the curve of urine NE versus body weight gain after 3 months on HE diet was 4-fold greater in DIO- than in DR-prone rats. After 3 months on the HE diet, there was no statistical relationship between 24-hour urine NE and body weight or prior body weight gain in DIO or DR rats. Six-month-old DIO-prone rats had 126% and 128% more urine NE and gained 112% and 232% more weight after 3 months on HE diet than DR-prone and chow-fed rats, respectively. Only DIO-prone rats showed a correlation (r=0.879; p=0.05) between urine NE levels and subsequent weight gain on HE diet. Thus, 3- or 6-month-old DIO- and DR-prone rats can be identified by their 24-hour basal urine NE levels but not sucrose preference prior to HE diet exposure. While this may suggest higher basal sympathetic activity in DIO-prone rats, other explanations are possible.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 93%

Sympathetic Activity, Age, Sucrose Preference, and Diet‐Induced Obesity

Levin

1993

Obesity Research

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“…A basic understanding of the neurochemical and metabolic traits which predispose animals to become DR or DIO is best gained by investigations carried out before dietary intervention unalterably changes these parameters. There are several phenotypic markers which allow a statistical prediction of future weight gain patterns of chow-fed rats when they are later fed HE diets (2, 10,15,19,20,25). We have used such predictive tests to separate DR-from DIO-prone rats before HE diet exposure.…”

Section: Introductionmentioning

confidence: 99%

Plasticity of Brain α‐Adrenoceptors During the Development of Diet‐Induced Obesity in the Rat

Levin

Hamm

1994

Obesity Research

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Male Sprague-Dawley rats, which are prone to develop diet-induced obesity (DIO) on a high energy (HE) diet can be separated from rats which are diet-resistant (DR) by several prospective tests. Using such tests, chow-fed DRl-prone rats have higher binding of 3H paraminoclonidine (PAC) to brain alpha2-adrenoceptors than do DIO-prone rats. These differences disappear after 3 months on a HE diet. To study the predictive value of these tests and possible associated changes in presynaptic membrane composition, brain alpha3(1-) (1nM 3H prazosin) and (alpha2-adrenoceptor (1nM) 3-H PAC) binding and synaptosomal fatty acid composition were assessed in 3-month-old male rats separated by weight gain into DR and DIO groups after 1 month on a HE diet. DIO had comparable total caloric intake but gained 30% and 43% more weight and were hyperinsulinemic compared to DR and chow-fed rats, respectively. After 1 month on a HE diet, DR rats still had 15%-53% higher 3H PAC binding than DIO and/or chow-fed rats in 14 of 16 brain areas assessed. A phenotype effect was present primarily in the amygdala where DR rats had higher 3H PAC binding than DIO rats. A diet effect was seen in some hypothalamic nuclei where both DR and DIO rats had higher 3H PAC binding than chow-fed rats. Conversely, DIO rats had 14%-21% higher 3H prazosin binding than DR rats in 3 brain areas. Changes in brain synaptosomal membranes' fatty acids reflected both phenotype and diet effects. Thus, while diet composition affects presynaptic membrane composition and alpha2-adrenoceptor binding in both DR and DIO rats, the predominance of plasticity of these parameters is limited to the brains of DR rats. This suggests that such plasticity may be an important determinant of the ability to resist the development of diet-induced obesity on a HE diet.

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“…In short, irrespective of its etiology, in obese animals preference is biased toward higher concentrations of sucrose 36,145,146 . Although this exaggerated preference probably results from both orosensory and postingestive factors, the taste component is sufficient for expression of the effect 145,147,148 . Furthermore, we reviewed functional and anatomical data implicating the PBN in the hedonic processing of taste information.…”

Section: Parabrachial Coding Of Sucrose Is Altered In Obese Ratsmentioning

confidence: 99%

“…36,145,146 Although this exaggerated preference probably results from both orosensory and postingestive factors, the taste component is sufficient for expression of the effect. 145,147,148 Furthermore, we reviewed functional and anatomical data implicating the PBN in the hedonic processing of taste information. Therefore, the discussion that follows is restricted to specific points related to the particular model we used.…”

Section: Parabrachial Coding Of Sucrose Is Altered In Obese Ratsmentioning

confidence: 99%

Parabrachial Coding of Sapid Sucrose:

Hajnal

Norgren

Kovács

2009

Annals of the New York Academy of Sciences

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Cumulative evidence in rats suggests that the pontine parabrachial nucleus (PBN) is necessary for assigning hedonic value to taste stimuli. In a series of studies, our laboratory has investigated the parabrachial coding of sapid sucrose in normal and obese rats. First, using chronic microdialysis, we demonstrated that sucrose intake increases dopamine release in the nucleus accumbens, an effect that is dependent on oral stimulation and on concentration. The dopamine response was independent of the thalamocortical gustatory system, but was blunted substantially by lesions of the PBN. Similar lesions of the PBN but not the thalamic taste relay diminished cFos activation by sucrose ingestion in the nucleus accumbens. Recent single neuron recording studies demonstrated that processing of sucrose-evoked activity in the PBN is altered in the Otsuka Long Evans Tokushima Fatty (OLETF) rats that develop obesity due to chronic overeating and express increased avidity to sweet. Compared with lean controls, taste neurons in OLETF rats had reduced overall sensitivity to sucrose and altered concentration responses: decreased responses to lower and augmented responses to higher concentrations. The decreased sensitivity to sucrose was specific to NaCl-best neurons that also responded to sucrose, but the concentration effects were carried by the sucrose-specific neurons. Collectively, these findings support the hypothesis that the PBN enables taste stimuli to engage the reward system and, in doing so, influences food intake and body weight regulation. Obesity, in turn, may further alter the gustatory code via forebrain connections to the taste relays or hormonal changes consequent to weight gain.

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Sensory responses, dietary-induced obesity and biochemical values in Sprague-Dawley rats

Cited by 7 publications

References 14 publications

Sympathetic Activity, Age, Sucrose Preference, and Diet‐Induced Obesity

Sympathetic Activity, Age, Sucrose Preference, and Diet‐Induced Obesity

Plasticity of Brain α‐Adrenoceptors During the Development of Diet‐Induced Obesity in the Rat

Parabrachial Coding of Sapid Sucrose:

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