Accelerometer-Measured Versus Self-Reported Physical Activity Levels and Sedentary Behavior in Women Before and 9 Months After Roux-en-Y Gastric Bypass

Berglind, Daniel; Willmer, Mikaela; Tynelius, Per; Ghaderi, Ata; Näslund, Erik; Rasmussen, Finn

doi:10.1007/s11695-015-1971-5

Cited by 48 publications

(42 citation statements)

References 44 publications

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“…Collectively, these data suggest that reductions in dopamine function accompanying obesity could persist following weight loss. This notion is consistent with findings that physical inactivity levels remained high in obese humans months after weight loss (69–71), raising the question whether “physical activity resistance” exists temporarily/permanently after weight loss.…”

Section: Obesity and Dopaminergic Dysregulationsupporting

confidence: 89%

Running from Disease: Molecular Mechanisms Associating Dopamine and Leptin Signaling in the Brain with Physical Inactivity, Obesity, and Type 2 Diabetes

Ruegsegger

Booth

2017

Front. Endocrinol.

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Physical inactivity is a primary contributor to diseases such as obesity, cardiovascular disease, and type 2 diabetes. Accelerometry data suggest that a majority of US adults fail to perform substantial levels of physical activity needed to improve health. Thus, understanding the molecular factors that stimulate physical activity, and physical inactivity, is imperative for the development of strategies to reduce sedentary behavior and in turn prevent chronic disease. Despite many of the well-known health benefits of physical activity being described, little is known about genetic and biological factors that may influence this complex behavior. The mesolimbic dopamine system regulates motivating and rewarding behavior as well as motor movement. Here, we present data supporting the hypothesis that obesity may mechanistically lower voluntary physical activity levels via dopamine dysregulation. In doing so, we review data that suggest mesolimbic dopamine activity is a strong contributor to voluntary physical activity behavior. We also summarize findings suggesting that obesity leads to central dopaminergic dysfunction, which in turn contributes to reductions in physical activity that often accompany obesity. Additionally, we highlight examples in which central leptin activity influences physical activity levels in a dopamine-dependent manner. Future elucidation of these mechanisms will help support strategies to increase physical activity levels in obese patients and prevent diseases caused by physical inactivity.

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Section: Obesity and Dopaminergic Dysregulationsupporting

confidence: 89%

Running from Disease: Molecular Mechanisms Associating Dopamine and Leptin Signaling in the Brain with Physical Inactivity, Obesity, and Type 2 Diabetes

Ruegsegger

Booth

2017

Front. Endocrinol.

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“…Taken together, the results of our cross‐sectional study as well as the findings from the aforementioned longitudinal studies (Afshar et al , ; Berglind et al , ; King et al , ) indicate enormous barriers for bariatric surgery patients to be physically active. An alternative explanation for the low PA can be found in the individual's temperament that is considered to be relatively stable over time and that can influence habitual PA (Allen, Magee, Vella, & Laborde, ; Brunes, Augestad, & Gudmundsdottir, ; Claes & Müller, ; Rhodes & Smith, ).…”

Section: Introductionsupporting

confidence: 76%

“…According to a longitudinal multicenter study conducted in the USA, most patients continue to have a sedentary lifestyle following bariatric surgery despite modest increases in PA (King et al , ). Lately, longitudinal studies from the UK and Sweden did not find significant increases in objectively measured PA after bariatric surgery (Afshar et al , ; Berglind et al , ).…”

Section: Introductionmentioning

confidence: 99%

Physical Activity in Bariatric Surgery Patients: Does Temperament Matter?

Gruner-Labitzke¹,

Claes

Bartsch

et al. 2017

Euro Eating Disorders Rev

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Questionnaire-Short Form, and the Patient Health Questionnaire-depression scale were 5 administered to 70 pre-and 73 postoperative patients. They were categorized as being 6 physically "active" if they accumulated ≥8000 steps/day based on objective monitoring. 7Results: Regressions adjusted for gender, age, BMI, and depression suggested an association 8 between lower BMI and more PA in both groups. In postoperative patients, lower age and 9higher BIS -but not BAS -reactivity were related to PA. There was a significant interaction 10 between BMI and BIS suggesting that low BMI was only associated with more PA in patients 11 with high BIS compared to low BIS sensitivity. Discussion: The results indicate that in 12 postoperative patients with anxious temperament lower BMI is associated with more PA. This 13 finding needs further investigation within longitudinal studies. 14 15

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“…Additionally, increased adiposity is hypothesized to contribute to low activity levels in people with obesity (Ekkekakis and Lind, 2006; Westerterp, 1999), although this idea is difficult to test directly. Interestingly, people who lose weight either through diet (de Boer et al, 1986; de Groot et al, 1989; Martin et al, 2007; Redman et al, 2009) or bariatric surgery (Berglind et al, 2015a; Berglind et al, 2015b; Bond et al, 2010; Ramirez-Marrero et al, 2014) do not increase their activity levels, arguing against the weight of adiposity causing their inactivity. Here, we investigated the hypothesis that diet-induced obesity causes physical inactivity via deficits in striatal DA transmission.…”

Section: Discussionmentioning

confidence: 99%

Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity

et al. 2017

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Summary Obesity is associated with physical inactivity, which exacerbates the health consequences of weight gain. However, the mechanisms that mediate this association are unknown. We hypothesized that deficits in dopamine signaling contribute to physical inactivity in obesity. To investigate this, we quantified multiple aspects of dopamine signaling in lean and obese mice. We found that D2-type receptor (D2R) binding in the striatum, but not D1-type receptor binding or dopamine levels, was reduced in obese mice. Genetically removing D2Rs from striatal medium spiny neurons was sufficient to reduce motor activity in lean mice, while restoring Gi signaling in these neurons increased activity in obese mice. Surprisingly, while mice with low D2Rs were less active, they were not more vulnerable to diet-induced weight gain than control mice. We conclude that deficits in striatal D2R signaling contribute to physical inactivity in obesity, but inactivity is more a consequence than a cause of obesity.

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Accelerometer-Measured Versus Self-Reported Physical Activity Levels and Sedentary Behavior in Women Before and 9 Months After Roux-en-Y Gastric Bypass

Abstract: Pre- to post-RYGB surgery increases in self-reported PA were not confirmed by accelerometer-measured PA. Thus, health care workers should use objective measures of PA in patients undergoing RYGB, in order to assess whether patients achieve sufficient levels of PA.

Cited by 48 publications

References 44 publications

Running from Disease: Molecular Mechanisms Associating Dopamine and Leptin Signaling in the Brain with Physical Inactivity, Obesity, and Type 2 Diabetes

Running from Disease: Molecular Mechanisms Associating Dopamine and Leptin Signaling in the Brain with Physical Inactivity, Obesity, and Type 2 Diabetes

Physical Activity in Bariatric Surgery Patients: Does Temperament Matter?

Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity

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