Increased caloric intake after a high-fat preload: Relation to circulating triglycerides and orexigenic peptides

The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.
Physiology & Behavior (Impact Factor: 2.98). 06/2007; 91(1):142-53. DOI: 10.1016/j.physbeh.2007.02.002
Source: PubMed


To investigate mechanisms that mediate the greater food intake induced by a fat-rich diet, the present study tested an acute "preload-to-test meal" paradigm in normal-weight rats. In this paradigm, the rats were given a small high-fat (HF) compared to low-fat (LF) preload and, after an intermeal interval, allowed to consume freely on a subsequent test meal. Modified versions of this paradigm were tested to determine the robustness of the greater caloric intake induced by the HF preload while standardizing the test protocol. A HF preload of 10-15 kcals, compared to an equicaloric LF preload, significantly increased food intake by 40-50% in the subsequent test meal. This effect, a 4-6 kcal increase, was observed with HF preloads equal in energy density and palatability to the LF preloads. It was evident with preloads or test meals that were liquid or solid, preloads that were injected, test meals that had variable fat content, and natural intermeal intervals of 60-120 min. This overeating after a HF preload was invariably associated with a 2- to 3-fold increase in circulating levels of triglycerides (TG), with no change in leptin or insulin. It was also accompanied by increased expression of the orexigenic peptides, galanin in the paraventricular nucleus and orexin in the perifornical lateral hypothalamus. Moreover, if given repeatedly over several days, the HF compared to equicaloric LF preload significantly increased 24-h food intake. These results establish a protocol for studying the phenomenon of increased feeding on a HF diet under controlled conditions and suggest possible underlying mechanisms involving circulating lipids and orexigenic peptides.

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    • "Although there was no statistically significance, serum TG levels were decreased in females treated with Korean red ginseng extract. The changes might be associated with slightly decreased food consumption in females because fat and carbohydrates in diet could affect serum TG levels (15,16). However, the slight changes were not seen in males or dose-dependent manner and there were no correlated histopathological findings; therefore, they are considered irrelevant to the test article treatment. "
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    ABSTRACT: Ginseng is a well-known traditional medicine used in Asian countries for several thousand years, and it is currently applied to medicine, cosmetics, and nutritional supplements due to its many healing and energygiving properties. It is well demonstrated that ginsenosides, the main ingredient of ginseng, produce a variety of pharmacological and therapeutic effects on central nerve system (CNS) disorders, cardiovascular disease, endocrine secretions, aging, and immune function. Korean red ginseng extract is a dietary supplement containing ginsenoside Rb1 and ginsenoside Rg1 extracted from Panax ginseng. While the pharmacokinetics and bioavailability of the extract have been well established, its toxicological properties remain obscure. Thus, four-week oral toxicity studies in rats were conducted to investigate whether Korean red ginseng extract could have a potential toxicity to humans. The test article was administered once daily by oral gavage to four groups of male and female Sprague-Dawley (SD) rats at dose levels of 0, 500, 1,000, and 2,000 mg/kg/day for four weeks. Neither deaths nor clinical symptoms were observed in any group during the experiment. Furthermore, no abnormalities in body weight, food consumption, ophthalmology, urinalysis, hematology, serum biochemistry, gross findings, organ weights, or histopathology were revealed related to the administration of the test article in either sex of any dosed group. Therefore, a target organ was not determined in this study, and the no observed adverse effect level (NOAEL) of Korean red ginseng extract was established to be 2,000 mg/kg/day.
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    • "Corroborating these data, we observed that serum TG levels showed circadian variation and were increased in the hypercaloric diet-induced obesity group, suggesting that obesity results in desynchronization of the temporal pattern of serum TG levels. The increase in serum TG levels may be associated with the dysregulation of energy balance, and may act to promote overeating, thus leading to an increase in body weight and attendant metabolic disturbances, which can trigger obesity [29]. Elevated TG levels can also have an impact on brain mechanisms that control feeding, and may contribute to fat-induced hyperphagia [6]. "
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    ABSTRACT: Disruption of the circadian system can lead to metabolic dysfunction as a response to environmental alterations. This study assessed the effects of the association between obesity and chronic stress on the temporal pattern of serum levels of adipogenic markers and corticosterone in rats. We evaluated weekly weight, delta weight, Lee index, and weight fractions of adipose tissue (mesenteric, MAT; subcutaneous, SAT; and pericardial, PAT) to control for hypercaloric diet-induced obesity model efficacy. Wistar rats were divided into four groups: standard chow (C), hypercaloric diet (HD), stress plus standard chow (S), and stress plus hypercaloric diet (SHD), and analyzed at three time points: ZT0, ZT12, and ZT18. Stressed animals were subjected to chronic stress for 1h per day, 5 days per week, during 80 days. The chronic exposure to a hypercaloric diet was an effective model for the induction of obesity and metabolic syndrome, increasing delta weight, Lee index, weight fractions of adipose tissue, and triglycerides and leptin levels. We confirmed the presence of a temporal pattern in the release of triglycerides, corticosterone, leptin, and adiponectin in naïve animals. Chronic stress reduced delta weight, MAT weight, and levels of triglycerides, total cholesterol, and leptin. There were interactions between chronic stress and obesity and serum total cholesterol levels, between time points and obesity and adiponectin and corticosterone levels, and between time points and chronic stress and serum leptin levels. In conclusion, both parameters were able to desynchronize the temporal pattern of leptin and triglyceride release, which could contribute to the development of metabolic diseases such as obesity and metabolic syndrome.
    Full-text · Article · Oct 2013 · Peptides
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    • "After consuming palatable food, OX levels are similarly elevated. With high-fat compared to low-fat, high-carbohydrate food, OX gene expression, and OX-A peptide levels are elevated after a single meal or up to three weeks on the diet [90–92], with longer periods of exposure leading to compensatory decreases in OX [93]. Interestingly, this fat-induced increase in OX may occur more from saturated than unsaturated fat, as consumption of a lard-based diet leads to higher OX mRNA levels than does that of a fish oil-based diet [94, 95]. "
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