Decreased responsiveness to dietary fat in Otsuka  Long-Evans Tokushima fatty rats lacking CCK-A receptors

Schwartz, Gary J.; Whitney, Andrew C.; Skoglund, Chris; Castonguay, Thomas W.; Moran, Timothy H.

doi:10.1152/ajpregu.1999.277.4.r1144

Cited by 67 publications

(73 citation statements)

References 16 publications

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“…OLETF female rats lost fat during the lactation period, from all the three examined tissues. In the middle of the lactation period and during the transition toward weaning (days [15][16][17][18][19][20][21][22], OLETF dams had reduced weight fat tissues that did not differ from those of LETO controls in the same lactation stage. In contrast, 8 weeks PW OLETF dams gained fats, appearing to re-achieve the same amount as observed in NP.…”

Section: Adipose Tissuesmentioning

confidence: 89%

“…19 OLETF male rats fail to compensate for fat calories. 20 Leptin acts at the level of the hypothalamus to decrease the synthesis and secretion of NPY and agouti-related peptide (AGRP) 8 and decreases the synthesis of the prepropeptide pre-opiomelanocortin (POMC). OLETF rats do not appear to have a primary deficit involving arcuate nucleus NPY or POMC signaling but rather a primary deficit in DMH hypothalamic NPY signaling, with upregulated levels of DMH NPY that may contribute to their hyperphagia and obesity.…”

Section: Introductionmentioning

confidence: 99%

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Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

et al. 2008

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Objective: To understand the adaptation to lactation of obese rats, by studying the interplay among the gut hormone cholecystokinin (CCK), the adiposity hormone leptin and the affiliation hormone oxytocin in modulating body mass and fat storage. Design: Strain differences were examined between Otsuka Long Evans Tokushima Fatty (OLETF) rats lacking expression of functional CCK-1 receptors and Long Evans Tokushima Otsuka (LETO) controls, tested as nulliparous dams, at the 7 and 15th lactation day, at weaning (lactation day 22) or 8 weeks postweaning. Measurements: We measured body mass, fat pads (brown, retroperitoneal and inguinal) and inguinal adipocytes. Plasma levels of leptin and oxytocin were determined. Results: Fat depots of LETO female rats were larger during lactation compared to the levels found in postweaning and nulliparous female rats. LETO female rats gained weight and accumulated fat during pregnancy and lactation, returning to their normal fat levels postweaning. In contrast, OLETF female rats presented lower body weight and fat depots during the lactation period than nulliparous dams, and regained the weight and fat postweaning. Plasma leptin and oxytocin were highly correlated and followed the same pattern. OLETF leptin levels were highly correlated with fat depot and inguinal cell surface. No significant correlation was found for LETO parameters. Conclusions: Pregnancy and lactation are energy-consuming events, which naturally induce female rats to increase food intake and accumulate fat. When challenged by the demands of rapidly growing preobese OLETF pups, OLETF dams' fat stores are reduced to lean, LETO levels. During lactation, sensitivity of the oxytocinergic neurons descending from the paraventricular nuclei to the nucleus of the solitary tract to CCK is reduced. We theorized that this pathway is not available to OLETF female rats that lack functional CCK-1 receptors to mediate the signal. The current study contributes to the understanding of the female body's adaptation to lactation.

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Section: Adipose Tissuesmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

et al. 2008

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“…CCK may also act as a longer-term indicator of nutritional status: the CCK A receptor-knockout (OLETF) rat (but not the CCK A receptor-knockout mouse) is hyperphagic and obese (Moran et al 1998, Schwartz et al 1999. Chronic administration of both CCK antibodies and CCK A antagonists also results in weight gain in rodent models, although not with a significant increase in food intake (McLaughlin et al 1985, Meereis-Schwanke et al 1998.…”

Section: Proglucagon Productsmentioning

confidence: 99%

Appetite control

Wynne¹,

Stanley²,

McGowan³

et al. 2005

Journal of Endocrinology

475

403

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Our understanding of the physiological systems that regulate food intake and body weight has increased immensely over the past decade. Brain centres, including the hypothalamus, brainstem and reward centres, signal via neuropeptides which regulate energy homeostasis. Insulin and hormones synthesized by adipose tissue reflect the long-term nutritional status of the body and are able to influence these circuits. Circulating gut hormones modulate these pathways acutely and result in appetite stimulation or satiety effects. This review discusses central neuronal networks and peripheral signals which contribute energy homeostasis, and how a loss of the homeostatic process may result in obesity. It also considers future therapeutic targets for the treatment of obesity.

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“…Brain CCK receptor deficiency results in hyperphagia and decreased responsiveness to high fat diet in rats [18][19][20]. Dorsal medial hypothalamic CCK inhibits food intake for at least 22 h [21,22].…”

Section: Discussionmentioning

confidence: 99%

Overnight Access to Sugar Solutions Affects mRNA Expression of Several Neuropeptides in Different Hypothalamic Regions in Rats

Zhao¹,

Campbell²,

Tschiffely³

et al. 2015

JFNR

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It has been known for years that free access to sugar solutions can cause weight gain and/or obesity in rats. We recently reported that brief access to sugar solutions can affect the hypothalamic neuropeptides that help to regulate energy balance. In this paper, we present the results in which we examined the effects of these sugars on the expression of several neuropeptides within specific hypothalamic regions. We provided Sprague Dawley rats 24 h access to 15% solutions of glucose, fructose, sucrose or high fructose corn syrup (HFCS) and then dissected portions of the paraventricular hypothalamic nuclei (PVN), the ventromedial hypothalamus (VMH) and the lateral hypothalamus (LH). We then evaluated the expression of several neuropeptides in these tissues, all of which were previously shown to be influenced by free access to sugar solutions using PCR array. Of the four sugar solutions tested, only fructose decreased expression of cholecystokinin (CCK) significantly, and only in the PVN. Glucose and sucrose significantly increased the expression of Tumor Necrosis Factor α (TNF-α) only in the PVN. Fructose and sucrose decreased Growth Hormone (GH) in the VMH. Further analysis indicated that it was fructose intake that was negatively correlated with both CCK and GH expression. Rats that had access to sugar solutions consumed less chow but maintained control levels of total caloric intake. We conclude that 24 h free access to different sugars can influence the expression of several hypothalamic neuropeptides in different ways. Changes in the expression of these neuropeptides do not disrupt total daily energy intake immediately but may nevertheless contribute to the obesity caused by long term access to sugar solutions.

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Decreased responsiveness to dietary fat in Otsuka Long-Evans Tokushima fatty rats lacking CCK-A receptors

Cited by 67 publications

References 16 publications

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

Adaptation to lactation in OLETF rats lacking CCK-1 receptors: body weight, fat tissues, leptin and oxytocin

Appetite control

Overnight Access to Sugar Solutions Affects mRNA Expression of Several Neuropeptides in Different Hypothalamic Regions in Rats

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