Persistent effects of obesity: a neuroplasticity hypothesis

Matikainen‐Ankney, Bridget A.; Kravitz, Alexxai V.

doi:10.1111/nyas.13665

Cited by 46 publications

(37 citation statements)

References 245 publications

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“…In a recent study, Song et al [ 26 ] found that subjecting rats to a diet rich in fat produced an increase in the postoperative pain in them. This fact coincides with other similar studies evaluating other types of pain models such as inflammatory or neuropathic [ 39 , 40 ]. In addition, Song et al [ 26 ] demonstrated that a single week of a high-fat diet was not capable of producing obesity, but an increase in the pain response, although of lesser magnitude.…”

Section: Discussionsupporting

confidence: 92%

Effects of a Fat-Rich Diet on the Spontaneous Release of Acetylcholine in the Neuromuscular Junction of Mice

et al. 2020

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Western societies are facing a clear increase in the rate of obesity and overweight which are responsible for musculoskeletal pain. Some of the substances described in the environment of myofascial trigger points (MTrPs) are the same as those found in the skeletal muscle of obese people, such as cytokines. Furthermore, elevated neuromuscular neurotransmission has been associated with MTrPs. The main objective of this study is to assess whether obesity or overweight may be a facilitator of myofascial pain. The experiments were performed on male Swiss mice. One experimental group was given a typical “cafeteria” diet and another group a commercial high-fat diet for six weeks. Intramuscular adipocytes were assessed with Sudan III. The functional study was performed with electromyographic recording to determine the plaque noise and intracellular recording of miniature endplate potentials (MEPPs). The intake of a cafeteria diet showed the presence of more adipocytes in muscle tissue, but not with the fat-supplemented diet. Both experimental groups showed an increase in the plaque noise and an increase in the frequency of MEPPs that lasted several weeks after interrupting diets. In summary, the supply of a hypercaloric diet for six weeks in mice increases spontaneous neurotransmission, thus facilitating the development of MTrPs.

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Section: Discussionsupporting

confidence: 92%

Effects of a Fat-Rich Diet on the Spontaneous Release of Acetylcholine in the Neuromuscular Junction of Mice

et al. 2020

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“…It is well-known that the central nervous system regulates energy homeostasis and obesity (Gautron et al, 2015), and several studies suggest that brain neuroplasticity underlies chronic pain (Apkarian et al, 2009;Mansour et al, 2014;Doan et al, 2015;Descalzi et al, 2017) and obesity (Matikainen-Ankney and Kravitz, 2018;Mattson et al, 2018). The nucleus accumbens (NAc) has been investigated as having a critical role in modulating chronic pain in humans and animal models (Martikainen et al, 2015;Ren et al, 2015;Benarroch, 2016;Schwartz et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

et al. 2020

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Recent findings from rodent studies suggest that high-fat diet (HFD) increases hyperalgesia independent of obesity status. Furthermore, weight loss interventions such as voluntary physical activity (PA) for adults with obesity or overweight was reported to promote pain reduction in humans with chronic pain. However, regardless of obesity status, it is not known whether HFD intake and sedentary (SED) behavior is underlies chronic pain susceptibility. Moreover, differential gene expression in the nucleus accumbens (NAc) plays a crucial role in chronic pain susceptibility. Thus, the present study used an adapted model of the inflammatory prostaglandin E2 (PGE2)induced persistent hyperalgesia short-term (PH-ST) protocol for mice, an HFD, and a voluntary PA paradigm to test these hypotheses. Therefore, we performed an analysis of differential gene expression using a transcriptome approach of the NAc. We also applied a gene ontology enrichment tools to identify biological processes associated with chronic pain susceptibility and to investigate the interaction between the factors studied: diet (standard diet vs. HFD), physical activity behavior (SED vs. PA) and PH-ST (PGE vs. saline). Our results demonstrated that HFD intake and sedentary behavior promoted chronic pain susceptibility, which in turn was prevented by voluntary physical activity, even when the animals were fed an HFD. The transcriptome of the NAc found 2,204 differential expression genes and gene ontology enrichment analysis revealed 41 biologic processes implicated in chronic pain susceptibility. Taking these biological processes together, our results suggest that genes related to metabolic and mitochondria stress were up-regulated in the chronic pain susceptibility group (SED-HFD-PGE), whereas genes related to neuroplasticity were up-regulated in the non-chronic pain susceptibility group (PA-HFD-PGE). These findings provide pieces of evidence that HFD intake and sedentary behavior provoked gene expression changes in the NAc related to promotion of chronic pain susceptibility, whereas voluntary physical activity provoked gene expression changes in the NAc related to prevention of chronic

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“…The reported desire of obese people to eat palatable food presents a different aspect for the disease—uncontrolled motivation to eat rewarding, palatable food. Indeed, differences between structures in the reward system of obese and nonobese humans or rodents have been described, and it was suggested that obese individuals share behavioral and neurobiological similarities with those addicted to drugs . When examining rats after chronic exposure to cocaine, two populations can be identified—those that are prone to develop addiction and those that are resistant (some mouse models of addiction also reveal populations that differ in their motivation to obtain the reward, but these are not yet established for cocaine).…”

Section: Introductionmentioning

confidence: 99%

Chronic calorie‐dense diet drives differences in motivated food seeking between obesity‐prone and resistant mice

et al. 2019

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Obesity results from overconsumption of energy, partly because of the inability to refrain from highly palatable rewarding foods. Even though palatable food is available to everyone, only a fraction of the population develops obesity. We previously showed that following chronic exposure to highly palatable food animals that gained the most weight also showed addictive-like motivation to seek for palatable food. An important question remains-is this extreme, addictive-like, motivation to consume palatable food the cause or the consequence of diet-induced obesity? Here, we show that obesity-prone (OP) mice exhibit higher motivation for palatable food consumption compared with obesity-resistant mice even before developing obesity, but that the full manifestation of this high motivation to eat is expressed only after chronic exposure to high-fat-high-sugar (HFHS) diet. HFHS diet also impairs performance in the operant food-seeking task selectively in OP mice, an impairment that persists even after 2 weeks of abstinence from HFHS food. Overall, our data suggest that while some aspects of food motivation are high in OP mice already before developing obesity, the chronic exposure to HFHS food accentuates it and drives the development of obesity.

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Persistent effects of obesity: a neuroplasticity hypothesis

Cited by 46 publications

References 245 publications

Effects of a Fat-Rich Diet on the Spontaneous Release of Acetylcholine in the Neuromuscular Junction of Mice

Effects of a Fat-Rich Diet on the Spontaneous Release of Acetylcholine in the Neuromuscular Junction of Mice

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

Chronic calorie‐dense diet drives differences in motivated food seeking between obesity‐prone and resistant mice

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