Increased Hypothalamic Inflammation Associated with the Susceptibility to Obesity in Rats Exposed to High-Fat Diet

Wang, Xiaoke; Ge, Aiguo; Cheng, Mengjie; Guo, Fangfang; Zhao, Min; Zhou, Xiaoqi; Liu, Liegang; Yang, Nianhong

doi:10.1155/2012/847246

Cited by 86 publications

(72 citation statements)

References 37 publications

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“…In the current study we found glucose and sucrose increased TNF-α mRNA expression. This effect is similar to that caused by high fat diet [30]. By contrast HFCS and fructose had no significant effect on TNF-α expression.…”

Section: Discussionsupporting

confidence: 77%

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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Section: Discussionsupporting

confidence: 77%

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

Zhao¹,

Campbell²,

Tschiffely³

et al. 2015

JFNR

View full text Add to dashboard Cite

show abstract

“…Wang suggests that once animals that have been made obese with a high fat diet are switched to a chow diet, the resulting elevated TNF expression does not return to levels of control (62). The importance of this finding here is that even if these animals were removed from the sugar diet they may still suffer from elevations of this inflammatory peptide.…”

Section: Tumor Necrosis Factormentioning

confidence: 83%

“…After the switch to a regular chow diet however, the upregulation of these TNF did not return to normal. This suggests that it may not be possible to reduce the inflammatory response that results from obesity (62). This is an important finding that may impact the way obesity therapies are designed.…”

Section: Tumor Necrosis Factormentioning

confidence: 99%

Effects of sugar solutions on hypothalamic appetite regulation

Colley¹,

Castonguay²

2015

Physiology & Behavior

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There are multiple hypotheses for the causes of the obesity epidemic. One such hypothesis is that dietary intake patterns have significantly shifted to include unprecedented amounts of refined sugar. We set out to determine some the unique metabolic changes that occur with initial exposure to dilute glucose, sucrose, high fructose corn syrup, or fructose solutions. Rats were given access to food, water and a sugar solution for 24 h, after which blood and tissues were collected. Fructose access (as opposed to other sugars investigated) resulted in a doubling of circulating triglycerides. Glucose consumption resulted in upregulation of 7 satiety related hypothalamic peptides whereas changes in gene expression were mixed for remaining sugars. Also, following multiple verification assays, 6 satiety related peptides were verified as being affected by sugar intake. These data provide evidence that not all sugars are equally effective in affecting the control of intake.

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“…Eating high fat chow also increases inflammation, both in adipose tissue and in the hypothalamus (Thaler et al, 2012; Wang et al, 2012). For example, the proinflammatory cytokines tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 are significantly increased in hypothalamic tissue from rats eating high fat chow (Maric et al, 2014; Wang et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Dietary supplementation with fish oil prevents high fat diet-induced enhancement of sensitivity to the locomotor stimulating effects of cocaine in adolescent female rats

Serafine

Labay

2016

Drug and Alcohol Dependence

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BACKGROUND Eating a diet high in fat can lead to obesity, chronic metabolic disease, and increased inflammation in both the central and peripheral nervous systems. Dietary supplements that are high in omega-3 polyunsaturated fatty acids can reduce or prevent these negative health consequences in rats. Eating high fat chow also increases the sensitivity of rats to behavioral effects of drugs acting on dopamine systems (e.g., cocaine), and this effect is greatest in adolescent females. METHODS The present experiment tested the hypothesis that dietary supplementation with fish oil prevents high fat chow induced increases in sensitivity to cocaine in adolescent female rats. Female Sprague-Dawley rats (post-natal day 25–27) ate standard laboratory chow (5.7% fat), high fat chow (34.4% fat), or high fat chow supplemented with fish oil (20% w/w). Cocaine dose dependently (1–17.8 mg/kg) increased locomotion and induced sensitization across 6 weeks of once-weekly testing in all rats; however, these effects were greatest in rats eating high fat chow. RESULTS Dietary supplementation with fish oil prevented enhanced locomotion and sensitization in rats eating high fat chow. There were no differences in inflammatory markers in plasma or the hypothalamus among dietary conditions. CONCLUSIONS These results demonstrate that dietary supplementation with fish oil can prevent high fat diet-induced sensitization to cocaine, but they fail to support the view that these effects are due to changes in proinflammatory cytokines. These data add to a growing literature on the relationship between diet and drug abuse and extend the potential health benefits of fish oil to stimulant drug abuse prevention.

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Increased Hypothalamic Inflammation Associated with the Susceptibility to Obesity in Rats Exposed to High-Fat Diet

Cited by 86 publications

References 37 publications

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

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

Effects of sugar solutions on hypothalamic appetite regulation

Dietary supplementation with fish oil prevents high fat diet-induced enhancement of sensitivity to the locomotor stimulating effects of cocaine in adolescent female rats

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