Insulin and extremity muscle mass in overweight and obese women

Leon, Benjamin; Jenkins, S.; Pepin, Kristen; Chaudhry, H. S.; Smith, Kevin P.; Zalos, Gloria; Miller, Bernard V.; Chen, Kong Y.; Remaley, Alan T.; Waclawiw, Myron A.; Sumner, Anne E.; Cannon, Richard O.

doi:10.1038/ijo.2013.45

Cited by 17 publications

(8 citation statements)

References 30 publications

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“…On the other hand, hyperinsulinemia in overweight/obese subjects is associated with increased extremity muscle mass, which is partially reversible with reduction in fasting insulin concentration, consistent with the stimulatory effects of insulin on skeletal muscle after treadmill exercise [575]. It is well known that insulin stimulates glycogen synthase (GS) through dephosphorylation of serine residues, and this effect is impaired in skeletal muscle from insulin-resistant obese subjects.…”

Section: Skeletal Musclementioning

confidence: 67%

Physiological Changes and Pathological Pain Associated with Sedentary Lifestyle-Induced Body Systems Fat Accumulation and Their Modulation by Physical Exercise

Verdú

Homs

Boadas-Vaello

2021

IJERPH

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A sedentary lifestyle is associated with overweight/obesity, which involves excessive fat body accumulation, triggering structural and functional changes in tissues, organs, and body systems. Research shows that this fat accumulation is responsible for several comorbidities, including cardiovascular, gastrointestinal, and metabolic dysfunctions, as well as pathological pain behaviors. These health concerns are related to the crosstalk between adipose tissue and body systems, leading to pathophysiological changes to the latter. To deal with these health issues, it has been suggested that physical exercise may reverse part of these obesity-related pathologies by modulating the cross talk between the adipose tissue and body systems. In this context, this review was carried out to provide knowledge about (i) the structural and functional changes in tissues, organs, and body systems from accumulation of fat in obesity, emphasizing the crosstalk between fat and body tissues; (ii) the crosstalk between fat and body tissues triggering pain; and (iii) the effects of physical exercise on body tissues and organs in obese and non-obese subjects, and their impact on pathological pain. This information may help one to better understand this crosstalk and the factors involved, and it could be useful in designing more specific training interventions (according to the nature of the comorbidity).

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Section: Skeletal Musclementioning

confidence: 67%

Physiological Changes and Pathological Pain Associated with Sedentary Lifestyle-Induced Body Systems Fat Accumulation and Their Modulation by Physical Exercise

Verdú

Homs

Boadas-Vaello

2021

IJERPH

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“… Fukushima et al (2016) using a 6-month mixed-exercise and nutritional intervention in 92 middle-aged obese women found that fasting insulin and glucose decreased in those whose SM mass index (kg/m 2 ) also decreased over the course of the intervention ( Fukushima et al, 2016 ). Leon et al (2013) also illustrated this point in 132 middle-aged women who participated in a 6-month diet and exercise program ( Leon et al, 2013 ). Before the intervention, the authors noted that appendicular SM mass was proportional to the level of obesity and was also proportionally related to fasting insulin levels.…”

Section: Narrative Literature Reviewmentioning

confidence: 99%

Exercising for Insulin Sensitivity – Is There a Mechanistic Relationship With Quantitative Changes in Skeletal Muscle Mass?

et al. 2021

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Skeletal muscle (SM) tissue has been repetitively shown to play a major role in whole-body glucose homeostasis and overall metabolic health. Hence, SM hypertrophy through resistance training (RT) has been suggested to be favorable to glucose homeostasis in different populations, from young healthy to type 2 diabetic (T2D) individuals. While RT has been shown to contribute to improved metabolic health, including insulin sensitivity surrogates, in multiple studies, a universal understanding of a mechanistic explanation is currently lacking. Furthermore, exercised-improved glucose homeostasis and quantitative changes of SM mass have been hypothesized to be concurrent but not necessarily causally associated. With a straightforward focus on exercise interventions, this narrative review aims to highlight the current level of evidence of the impact of SM hypertrophy on glucose homeostasis, as well various mechanisms that are likely to explain those effects. These mechanistic insights could provide a strengthened rationale for future research assessing alternative RT strategies to the current classical modalities, such as low-load, high repetition RT or high-volume circuit-style RT, in metabolically impaired populations.

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“…As obesity develops, there is an almost 1 : 1 increase in fat and lean mass . A significant portion of the increase in weight occurs in the form of skeletal muscle . Consequently, disposal of excess energy by more lean body mass could help to buffer the caloric overload in obese individuals.…”

Section: Overnutrition Vs Adipositymentioning

confidence: 99%

Adipose tissue and metabolic syndrome: too much, too little or neither

Grundy

2015

Eur J Clin Investigation

147

104

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Obesity is strongly associated with metabolic syndrome. Recent research suggests that excess adipose tissue plays an important role in development of the syndrome. On the other hand, persons with a deficiency of adipose tissue (e.g. lipodystrophy) also manifest the metabolic syndrome. In some animal models, expansion of adipose tissue pools mitigates adverse metabolic components (e.g. insulin resistance, hyperglycaemia and dyslipidemia). Hence, there are conflicting data as to whether adipose tissue worsens the metabolic syndrome or protects against it. This conflict may relate partly to locations of adipose tissue pools. For instance, lower body adipose tissue may be protective whereas upper body adipose tissue may promote the syndrome. One view holds that in either case, the accumulation of ectopic fat in muscle and liver is the driving factor underlying the syndrome. If so, there may be some link between adipose tissue fat and ectopic fat. But the mechanisms underlying this connection are not clear. A stronger association appears to exist between excessive caloric intake and ectopic fat accumulation. Adipose tissue may act as a buffer to reduce the impact of excess energy consumption by fat storage; but once a constant weight has been achieved, it is unclear whether adipose tissue influences levels of ectopic fat. Another mechanism whereby adipose tissue could worsen the metabolic syndrome is through release of adipokines. This is an intriguing mechanism, but the impact of adipokines on metabolic syndrome risk factors is uncertain. Thus, many potential connections between adipose tissue and metabolic syndrome remain to unravelled.

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Insulin and extremity muscle mass in overweight and obese women

Cited by 17 publications

References 30 publications

Physiological Changes and Pathological Pain Associated with Sedentary Lifestyle-Induced Body Systems Fat Accumulation and Their Modulation by Physical Exercise

Physiological Changes and Pathological Pain Associated with Sedentary Lifestyle-Induced Body Systems Fat Accumulation and Their Modulation by Physical Exercise

Exercising for Insulin Sensitivity – Is There a Mechanistic Relationship With Quantitative Changes in Skeletal Muscle Mass?

Adipose tissue and metabolic syndrome: too much, too little or neither

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