Weight loss with exercise improves muscle architecture and progenitor cell populations compared to weight loss alone in mice with preneoplastic colorectal lesions

Author(s):  
Sophia Roubos ◽  
Donna D’Souza ◽  
Diego Hernández-Saavedra ◽  
Guanying Xu ◽  
Nicolas Collao ◽  
...  

Weight loss and exercise reduce colorectal cancer (CRC) risk in persons with obesity. Whether weight loss and exercise effect myofibre characteristics and muscle stem/progenitor cell populations in mice with preneoplastic colorectal lesions, a model of CRC risk, is unknown. To address this gap, male C57Bl/6J mice were fed a high-fat diet (HFD) to induce obesity or a control (CON) diet prior to azoxymethane injection to induce preneoplastic colorectal lesions. The HFD group was then randomized to weight loss conditions that included (1) switching to the CON diet only (HFD-SED) or switching to the CON diet with treadmill exercise training (HFD-EX). Average myofibre cross-sectional area was not different between groups. There were more smaller-sized fibers in HFD-EX (p<0.05 vs. CON), and more fibrosis in HFD-SED (p<0.05 vs. HFD-EX and CON). There was a trend for more committed (Pax7+MyoD+) myoblasts (p=0.059) and more fibro-adipogenic progenitors (FAPs) in HFD-EX (p<0.05 vs. CON). Additionally, the canonical pro-inflammatory marker p-NF-κB, was markedly reduced in the insterstitium of HFD-EX (p<0.05 vs. CON and HFD-SED). Our findings suggest that in mice with preneoplastic colorectal lesions, HFD followed by weight loss with exercise, reduces muscle fibrosis and results in a higher content of muscle stem/progenitor cells. Novelty Bullets: • Exercise improves muscle architecture in mice with preneoplastic colorectal lesion • Exercise increases fibro/adipogenic progenitors and reduces inflammatory signaling in mice with preneoplastic colorectal lesions

Author(s):  
Jun-Won Heo ◽  
Su-Zi Yoo ◽  
Mi-Hyun No ◽  
Dong-Ho Park ◽  
Ju-Hee Kang ◽  
...  

Obesity is characterized by the induction of skeletal muscle remodeling and mitochondria-mediated apoptosis. Exercise has been reported as a positive regulator of skeletal muscle remodeling and apoptosis. However, the effects of exercise on skeletal muscle remodeling and mitochondria-mediated apoptosis in obese skeletal muscles have not been clearly elucidated. Four-week-old C57BL/6 mice were randomly assigned into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and HFD plus exercise groups (HFD + EX). After obesity was induced by 20 weeks of 60% HFD feeding, treadmill exercise was performed for 12 weeks. Exercise ameliorated the obesity-induced increase in extramyocyte space and a decrease in the cross-sectional area of the skeletal muscle. In addition, it protected against increases in mitochondria-mediated apoptosis in obese skeletal muscles. These results suggest that exercise as a protective intervention plays an important role in regulating skeletal muscle structure and apoptosis in obese skeletal muscles.


2011 ◽  
Vol 301 (5) ◽  
pp. R1267-R1280 ◽  
Author(s):  
Andrew C. Shin ◽  
R. Leigh Townsend ◽  
Laurel M. Patterson ◽  
Hans-Rudolf Berthoud

Cross-sectional studies in both humans and animals have demonstrated associations between obesity and altered reward functions at the behavioral and neural level, but it is unclear whether these alterations are cause or consequence of the obese state. Reward behaviors were quantified in male, outbred Sprague-Dawley (SD) and selected line obesity-prone (OP) and obesity-resistant (OR) rats after induction of obesity by high-fat diet feeding and after subsequent loss of excess body weight by chronic calorie restriction. As measured by the brief access lick and taste-reactivity paradigms, both obese SD and OP rats “liked” low concentrations of sucrose and corn oil less, but “liked” the highest concentrations more, compared with lean rats, and this effect was fully reversed by weight loss in SD rats. Acute food deprivation was unable to change decreased responsiveness to low concentrations but eliminated increased responsiveness to high concentrations in obese SD rats, and leptin administration in weight-reduced SD rats shifted concentration-response curves toward that seen in the obese state in the brief access lick test. “Wanting” and reinforcement learning as assessed in the incentive runway and progressive ratio lever-pressing paradigms was paradoxically decreased in both obese (compared with lean SD rats) and OP (compared with OR rats). Thus, reversible, obesity-associated, reduced “liking” and “wanting” of low-calorie foods in SD rats suggest a role for secondary effects of the obese state on reward functions, while similar differences between select lines of OP and OR rats before induction of obesity indicate a genetic component.


2019 ◽  
Vol 26 (1) ◽  
pp. 10-20
Author(s):  
Maija Huttunen-Lenz ◽  
Sylvia Hansen ◽  
Thomas Meinert Larsen ◽  
Pia Christensen ◽  
Mathijs Drummen ◽  
...  

Abstract. Individuals at risk of Type 2 Diabetes are advised to change health habits. This study investigated how the PREMIT behavior modification intervention and its association with socio-economic variables influenced weight maintenance and habit strength in the PREVIEW study. Overweight adults with pre-diabetes were enrolled ( n = 2,224) in a multi-center RCT including a 2-month weight-loss phase and a 34-month weight-maintenance phase for those who lost ≥ 8% body weight. Initial stages of the PREMIT covered the end of weight-loss and the beginning of weight-maintenance phase (18 weeks). Cross-sectional and longitudinal data were explored. Frequent PREMIT sessions attendance, being female, and lower habit strength for poor diet were associated with lower weight re-gain. Being older and not in employment were associated with lower habit strength for physical inactivity. The PREMIT appeared to support weight loss maintenance. Younger participants, males, and those in employment appeared to struggle more with inactivity habit change and weight maintenance.


2019 ◽  
Vol 14 (4) ◽  
pp. 305-319 ◽  
Author(s):  
Marietta Herrmann ◽  
Franz Jakob

The bone marrow hosts skeletal progenitor cells which have most widely been referred to as Mesenchymal Stem or Stromal Cells (MSCs), a heterogeneous population of adult stem cells possessing the potential for self-renewal and multilineage differentiation. A consensus agreement on minimal criteria has been suggested to define MSCs in vitro, including adhesion to plastic, expression of typical surface markers and the ability to differentiate towards the adipogenic, osteogenic and chondrogenic lineages but they are critically discussed since the differentiation capability of cells could not always be confirmed by stringent assays in vivo. However, these in vitro characteristics have led to the notion that progenitor cell populations, similar to MSCs in bone marrow, reside in various tissues. MSCs are in the focus of numerous (pre)clinical studies on tissue regeneration and repair.Recent advances in terms of genetic animal models enabled a couple of studies targeting skeletal progenitor cells in vivo. Accordingly, different skeletal progenitor cell populations could be identified by the expression of surface markers including nestin and leptin receptor. While there are still issues with the identity of, and the overlap between different cell populations, these studies suggested that specific microenvironments, referred to as niches, host and maintain skeletal progenitor cells in the bone marrow. Dynamic mutual interactions through biological and physical cues between niche constituting cells and niche inhabitants control dormancy, symmetric and asymmetric cell division and lineage commitment. Niche constituting cells, inhabitant cells and their extracellular matrix are subject to influences of aging and disease e.g. via cellular modulators. Protective niches can be hijacked and abused by metastasizing tumor cells, and may even be adapted via mutual education. Here, we summarize the current knowledge on bone marrow skeletal progenitor cell niches in physiology and pathophysiology. We discuss the plasticity and dynamics of bone marrow niches as well as future perspectives of targeting niches for therapeutic strategies.


Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2341
Author(s):  
Conner W. Wallace ◽  
Nari S. Beatty ◽  
Sarah A. Hutcherson ◽  
Heather A. Emmons ◽  
Madison C. Loudermilt ◽  
...  

Diet-induced obesity reduces dopaminergic neurotransmission in the nucleus accumbens (NAc), and stressful weight loss interventions could promote cravings for palatable foods high in fat and sugar that stimulate dopamine. Activation of κ-opioid receptors (KORs) reduces synaptic dopamine, but contribution of KORs to lower dopamine tone after dietary changes is unknown. Therefore, the purpose of this study was to determine the function of KORs in C57BL/6 mice that consumed a 60% high-fat diet (HFD) for six weeks followed by replacement of HFD with a control 10% fat diet for one day or one week. HFD replacement induced voluntary caloric restriction and weight loss. However, fast-scan cyclic voltammetry revealed no differences in baseline dopamine parameters, whereas sex effects were revealed during KOR stimulation. NAc core dopamine release was reduced by KOR agonism after one day of HFD replacement in females but after one week of HFD replacement in males. Further, elevated plus-maze testing revealed no diet effects during HFD replacement on overt anxiety. These results suggest that KORs reduce NAc dopamine tone and increase food-related anxiety during dietary weight loss interventions that could subsequently promote palatable food cravings and inhibit weight loss.


Author(s):  
Ambreen Asghar ◽  
Tasleem Akhtar ◽  
Tayyeba Batool ◽  
Muhammad Babar Khawar ◽  
Sania Nadeem ◽  
...  

2021 ◽  
Author(s):  
Larissa Cristina Lins Berber ◽  
Mariana Silva Melendez-Araújo ◽  
Eduardo Yoshio Nakano ◽  
Kênia Mara Baiocchi de Carvalho ◽  
Eliane Said Dutra

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