Feeding Response to Mercaptoacetate in Osborne‐Mendel and S5B/PL Rats

Singer, Lori; York, David A.; Bray, George A.

doi:10.1002/j.1550-8528.1997.tb00580.x

Cited by 23 publications

(6 citation statements)

References 24 publications

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“…In addition, numerous differences in feeding behavior have been reported. The stimulation of food intake by ␤-mercaptoacetate, an inhibitor of fatty acid oxidation, is reduced in S5B/Pl rats compared with the response in OM rats, whereas the increase in food intake in response to 2-deoxy-D-glucose, an inhibitor of glucose use, is similar in both strains (6). Other data also suggest a difference in the response to fatty acids in the two strains.…”

Section: Introductionmentioning

confidence: 93%

Effects of a High‐Fat Diet and Strain on Hypothalamic Gene Expression in Rats

et al. 2002

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Effects of a high-fat diet and strain on hypothalamic gene expression in rats. Obes Res. 2002;10:1188 -1196. Objective: This study was designed to investigate whether dietary fat and genetic background might differentially alter the expression of hypothalamic genes involved in food intake. Research Methods and Procedures: Three-month-old Osborne-Mendel (OM) and S5B/Pl rats were fed either a high-fat or a low-fat diet for 14 days. mRNA for neuropeptide Y (NPY), corticotrophin-releasing hormone, NPY Y-1 receptor and Y-5 receptor, and serotonin 2c (5-HT2c) receptors were measured using Northern blotting or ribonuclease protection assays. Results: OM rats showed an increased expression of NPY and corticotrophin-releasing hormone compared with S5B/Pl rats. The expression of NPY-Y1 and -Y5 receptor mRNA was significantly higher in the hypothalamus of OM rats compared with S5B/Pl rats. The expression of 5HT-2c receptor mRNA was significantly reduced in both strains of rats eating a high-fat diet when compared with the animals eating the low-fat diet. Discussion: These data suggest that over activity of the NPY system may contribute to the development of obesity in OM rats and that expression of the 5HT-2c receptor gene may be modulated by dietary fat.

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Section: Introductionmentioning

confidence: 93%

Effects of a High‐Fat Diet and Strain on Hypothalamic Gene Expression in Rats

et al. 2002

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“…Studies in animals indicate that this increased food intake is predominately carbohydrate and/or protein but not fat, even when fat is the only available nutrient (Singer et al 1997). The peripheral effects of 2-mercaptoacetate are blocked by hepatic vagotomy, but the effects of methyl palmoxirate are not (Ritter & Taylor, 1989, 1990.…”

Section: Ketones Fatty Acids and Lipoproteinsmentioning

confidence: 99%

Afferent signals regulating food intake

2000

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Food intake is a regulated system. Afferent signals provide information to the central nervous system, which is the centre for the control of satiety or food seeking. Such signals can begin even before food is ingested through visual, auditory and olfactory stimuli. One of the recent interesting findings is the demonstration that there are selective fatty acid taste receptors on the tongue of rodents. The suppression of food intake by essential fatty acids infused into the stomach and the suppression of electrical signals in taste buds reflect activation of a K rectifier channel (K 1.5). In animals that become fat eating a high-fat diet the suppression of this current by linoleic acid is less than that in animals that are resistant to obesity induced by dietary fat. Inhibition of fatty acid oxidation with either mercaptoacetate (which blocks acetyl-CoA dehydrogenase) or methylpalmoxirate will increase food intake. When animals have a choice of food, mercaptoacetate stimulates the intake of protein and carbohydrate, but not fat. Afferent gut signals also signal satiety. The first of these gut signals to be identified was cholecystokinin (CCK). When CCK acts on CCK-A receptors in the gastrointestinal tract, food intake is suppressed. These signals are transmitted by the vagus nerve to the nucleus tractus solitarius and thence to higher centres including the lateral parabrachial nucleus, amygdala, and other sites. Rats that lack the CCK-A receptor become obese, but transgenic mice lacking CCK-A receptors do not become obese. CCK inhibits food intake in human subjects. Enterostatin, the pentapeptide produced when pancreatic colipase is cleaved in the gut, has been shown to reduce food intake. This peptide differs in its action from CCK by selectively reducing fat intake. Enterostatin reduces hunger ratings in human subjects. Bombesin and its human analogue, gastrin inhibitory peptide (also gastrin-insulin peptide), reduce food intake in obese and lean subjects. Animals lacking bombesin-3 receptor become obese, suggesting that this peptide may also be important. Circulating glucose concentrations show a dip before the onset of most meals in human subjects and rodents. When the glucose dip is prevented, the next meal is delayed. The dip in glucose is preceded by a rise in insulin, and stimulating insulin release will decrease circulating glucose and lead to food intake. Pyruvate and lactate inhibit food intake differently in animals that become obese compared with lean animals. Leptin released from fat cells is an important peripheral signal from fat stores which modulates food intake. Leptin deficiency or leptin receptor defects produce massive obesity. This peptide signals a variety of central mechanisms by acting on receptors in the arcuate nucleus and hypothalamus. Pancreatic hormones including glucagon, amylin and pancreatic polypeptide reduce food intake. Four pituitary peptides also modify food intake. Vasopressin decreases feeding. In contrast, injections of desacetyl melanocyte-stimulating hormone, growth hormone and prolactin are associated with increased food intake. Finally, there are a group of miscellaneous peptides that modulate feeding. β-Casomorphin, a heptapeptide produced during the hydrolysis of casein, stimulates food intake in experimental animals. In contrast, the other peptides in this group, including calcitonin, apolipoprotein A-IV, the cyclized form of histidyl-proline, several cytokines and thyrotropin-releasing hormone, all decrease food intake. Many of these peptides act on gastrointestinal or hepatic receptors that relay messages to the brain via the afferent vagus nerve. As a group they provide a number of leads for potential drug development.

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“…The OM rat is more insulin‐resistant compared to the S5B/P1 rat (5) and has an attenuated activity of the fatty acid‐sensitive K + channel in their taste buds (6). In addition, numerous differences in their response to feeding modulators have been reported (4,7,8,9). These have suggested that the hypothalamic areas are involved in the sensitivity of OM rats for the HF diet‐induced obesity (10).…”

Section: Introductionmentioning

confidence: 99%

Differential Expression of Leptin Receptor in High‐ and Low‐Fat‐Fed Osborne‐Mendel and S5B/Pl Rats

et al. 2000

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Differential expression of leptin receptor in high-and low-fat-fed OM and S5B/Pl rats. Obes Res. 2000; 8:467-474. Objective: The regulation of body weight and body composition involves input from genes and the environment. This interaction is demonstrated by the different susceptibility of Osborne-Mendel (OM) and S5B/P1 rat strains to obesity when offered a high-fat diet. In animals and humans, diet-induced obesity has been characterized by hyperleptinemia, which has been interpreted as evidence for leptin resistance. This investigation determined if altered expression of leptin receptors (ObR) in the hypothalamus could potentially contribute to altered sensitivity to dietinduced obesity between OM and S5B/Pl rats. Research Methods and Procedures: OM and S5B/Pl rats were fed high-fat (HF) or low-fat (LF) diets for 14 days. Ribonuclease protection assays and Western blotting were used to assay the levels of mRNA and protein, respectively, for short (ObR-S) and long (ObR-L) forms of the leptin receptor in the hypothalamus. Results: The mRNA encoding ObR-L, the predominant signaling form of the receptor, was higher in OM rats than in S5B/P1 rats (p Ͻ 0.01) both on HF and LF diets. No changes in ObR-L mRNA expression were observed in OM rats with diet, but, S5B/P1 rats showed a slight increase in the ObR-L on the LF diet. On the contrary, there were no changes in ObR-S mRNA expression due to diet or strain. Western blots showed that both the short and long forms of the receptor were increased on the LF diet, but there were no strain differences. OM and S5B/Pl rats had comparable leptin levels after maintenance on a LF diet (6.20 Ϯ 0.63 and 4.81 Ϯ 0.82 ng/mL, respectively). Serum leptin levels in OM rats were increased by the HF diet and were elevated 2-fold over those of their S5B/Pl counterparts. Discussion: These results suggest that a decrease in the levels of both the long form and short form of the receptor may contribute to the leptin resistance seen in HF-fed rats. These effects appear to be post-transcriptional, because equivalent changes were not observed in the expression of ObR-L and ObR-S mRNAs. They may be related to the increase in circulating leptin levels, suggesting that high serum leptin levels contribute to increased leptin resistance and subsequently lead to obesity. We conclude that downregulation of receptor protein levels is associated with hypothalamic leptin resistance of HF-fed rats.

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Feeding Response to Mercaptoacetate in Osborne‐Mendel and S5B/PL Rats

Cited by 23 publications

References 24 publications

Effects of a High‐Fat Diet and Strain on Hypothalamic Gene Expression in Rats

Effects of a High‐Fat Diet and Strain on Hypothalamic Gene Expression in Rats

Afferent signals regulating food intake

Differential Expression of Leptin Receptor in High‐ and Low‐Fat‐Fed Osborne‐Mendel and S5B/Pl Rats

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