Leptin responses to physical inactivity induced by simulated weightlessness

2000 ◽  
Vol 279 (3) ◽  
pp. R891-R898 ◽  
Author(s):  
Stéphane Blanc ◽  
Sylvie Normand ◽  
Christiane Pachiaudi ◽  
Monique Duvareille ◽  
Claude Gharib

Physical inactivity induced by head-down bed rest (HDBR) affects body composition (BC). Leptin is involved in BC regulation by acting on fuel homeostasis. We investigated whether leptin and counterregulatory hormone levels are affected by a 7-day HDBR. Fasting blood was sampled daily (0700) in males ( n = 8) and on alternating days in females ( n = 8) for measurements of leptin, insulin, norepinephrine (NE), epinephrine (Epi), growth hormone (GH), cortisol, nonesterified fatty acid (NEFA), and glucose. BC was measured by H2 18O dilution. Energy intake (men 10.5 ± 0.2 MJ/day, women 7.9 ± 0.3 MJ/day) and BC were unchanged by HDBR. Increased levels of leptin (men 40%, P = 0.003; women 20%, P = 0.050), insulin (men 34%, P= 0.018; women 25%, P = 0.022), and the insulin-to-glucose ratio (men 30%, P = 0.049; women 25%, P = 0.031) were noted. GH, NE, Epi, and cortisol levels were unaltered. NEFA dropped in both sexes, but glucose decreased only in women. In conclusion, HDBR increased leptin levels independently of stress response, changes in fat mass, energy intake, or gender. These changes were correlated to the insulin-resistance development in men. Further analyses are required, but the results have to be considered for longer HDBR periods with 1) the well-described drop in energy intake and 2) the BC changes.

2011 ◽  
Vol 111 (4) ◽  
pp. 1218-1224 ◽  
Author(s):  
John P. Thyfault ◽  
Rikke Krogh-Madsen

Physical inactivity likely plays a role in the development of insulin resistance and obesity; however, direct evidence is minimal and mechanisms of action remain unknown. Studying metabolic outcomes that occur after transitioning from higher to lower levels of physical activity is the best tool to answer these questions. Previous studies have successfully used more extreme models of inactivity, including bed rest, or the cessation of exercise in highly trained endurance athletes, to provide novel findings. However, these models do not accurately reflect the type of inactivity experienced by a large majority of the population. Recent studies have used a more applicable model in which active (∼10,000 steps/day), healthy young controls are asked to transition to an inactive lifestyle (∼1,500 steps/day) for a 14-day period. The transition to inactivity resulted in reduced insulin sensitivity and increased central adiposity. This review will discuss the outcomes of these studies, their implications for the cause/effect relationship between central adiposity and insulin resistance, and provide rationale for why inactivity induces these factors. In addition, the experimental challenges of directly linking acute responses to inactivity to chronic disease will also be discussed.


2016 ◽  
Vol 120 (6) ◽  
pp. 608-614 ◽  
Author(s):  
Signe Tellerup Nielsen ◽  
Nina Majlund Harder-Lauridsen ◽  
Fabiana Braga Benatti ◽  
Anne-Sophie Wedell-Neergaard ◽  
Mark Preben Lyngbæk ◽  
...  

Bed rest and physical inactivity are the consequences of hospital admission for many patients. Physical inactivity induces changes in glucose metabolism, but its effect on the incretin effect, which is reduced in, e.g., Type 2 diabetes, is unknown. To investigate how 8 days of strict bed rest affects the incretin effect, 10 healthy nonobese male volunteers underwent 8 days of strict bed rest. Before and after the intervention, all volunteers underwent an oral glucose tolerance test (OGTT) followed by an intravenous glucose infusion (IVGI) on the following day to mimic the blood glucose profile from the OGTT. Blood glucose, serum insulin, serum C-peptide, plasma incretin hormones [glucagon-like peptide (GLP-1) and glucose-dependent insulinotropic peptide (GIP)], and serum glucagon were measured serially during both the OGTT and the IVGI. The incretin effect is calculated as the relative difference between the area under the curve for the insulin response during the OGTT and that of the corresponding IVGI, respectively. Concentrations of glucose, insulin, C-peptide, and GIP measured during the OGTT were higher after the bed rest intervention (all P < 0.05), whereas there was no difference in the levels of GLP-1 and Glucagon. Bed rest led to a mean loss of 2.4 kg of fat-free mass, and induced insulin resistance evaluated by the Matsuda index, but did not affect the incretin effect ( P = 0.6). In conclusion, 8 days of bed rest induces insulin resistance, but we did not see evidence of an associated change in the incretin effect.


2010 ◽  
Vol 299 (5) ◽  
pp. E752-E763 ◽  
Author(s):  
A. C. Alibegovic ◽  
M. P. Sonne ◽  
L. Højbjerre ◽  
J. Bork-Jensen ◽  
S. Jacobsen ◽  
...  

Physical inactivity is a risk factor for insulin resistance. We examined the effect of 9 days of bed rest on basal and insulin-stimulated expression of genes potentially involved in insulin action by applying hypothesis-generating microarray in parallel with candidate gene real-time PCR approaches in 20 healthy young men. Furthermore, we investigated whether bed rest affected DNA methylation in the promoter region of the peroxisome proliferator-activated receptor-γ coactivator-1α ( PPARGC1A) gene. Subjects were reexamined after 4 wk of retraining. We found that bed rest induced insulin resistance and altered the expression of more than 4,500 genes. These changes were only partly normalized after 4 wk of retraining. Pathway analyses revealed significant downregulation of 34 pathways, predominantly those of genes associated with mitochondrial function, including PPARGC1A. Despite induction of insulin resistance, bed rest resulted in a paradoxically increased response to acute insulin stimulation in the general expression of genes, particularly those involved in inflammation and endoplasmatic reticulum (ER) stress. Furthermore, bed rest changed gene expressions of several insulin resistance and diabetes candidate genes. We also observed a trend toward increased PPARGC1A DNA methylation after bed rest. We conclude that impaired expression of PPARGC1A and other genes involved in mitochondrial function as well as a paradoxically increased response to insulin of genes involved in inflammation and ER stress may contribute to the development of insulin resistance induced by bed rest. Lack of complete normalization of changes after 4 wk of retraining underscores the importance of maintaining a minimum of daily physical activity.


2011 ◽  
Vol 111 (4) ◽  
pp. 1201-1210 ◽  
Author(s):  
Audrey Bergouignan ◽  
Floriane Rudwill ◽  
Chantal Simon ◽  
Stéphane Blanc

Although it is no longer debatable that sedentary behaviors are an actual cause of many metabolic diseases, the physiology of physical inactivity has been poorly investigated for this purpose. Along with microgravity, the physiological adaptations to spaceflights require metabolic adaptations to physical inactivity, and that is exceedingly well-simulated during the ground-based microgravity bed-rest analogs. Bed rest thus represents a unique model to investigate the mechanisms by which physical inactivity leads to the development of current societal chronic diseases. For decades, however, clinicians and physiologists working in space research have worked separately without taking full awareness of potential strong mutual questioning. This review summarizes the data collected over the last 60 years on metabolic adaptations to bed rest in healthy subjects. Our aim is to provide evidence that supports the hypothesis that physical inactivity per se is one of the primary causes in the development of metabolic inflexibility. This evidence will focus on four main tenants of metabolic inflexiblity: 1) insulin resistance, 2) impaired lipid trafficking and hyperlipidemia, 3) a shift in substrate use toward glucose, and 4) a shift in muscle fiber type and ectopic fat storage. Altogether, this hypothesis places sedentary behaviors upstream on the list of factors involved in metabolic inflexibility, which is considered to be a primary impairment in several metabolic disorders such as obesity, insulin resistance, and type 2 diabetes mellitus.


Author(s):  
William V Trim ◽  
Jean-Philippe Walhin ◽  
Francoise Koumanov ◽  
Anne Bouloumié ◽  
Mark A Lindsay ◽  
...  

Abstract Context Adipose tissue and physical inactivity both influence metabolic health and systemic inflammation, but how adipose tissue responds to chronic physical inactivity is unknown. Objective This work aimed to characterize the impact of chronic physical inactivity on adipose tissue in healthy, young males. Methods We collected subcutaneous adipose tissue from 20 healthy, young men before and after 60 days of complete bed rest with energy intake reduced to maintain energy balance and fat mass. We used RNA sequencing, flow cytometry, ex vivo tissue culture, and targeted protein analyses to examine adipose tissue phenotype. Results Our results indicate that the adipose tissue transcriptome, stromal cellular compartment, and insulin signaling protein abundance are largely unaffected by bed rest when fat mass is kept stable. However, there was an increase in the circulating concentration of several adipokines, including plasma leptin, which was associated with inactivity-induced increases in plasma insulin and absent from adipose tissue cultured ex vivo under standardized culture conditions. Conclusion Physical inactivity–induced disturbances to adipokine concentrations such as leptin, without changes to fat mass, could have profound metabolic implications outside a clinical facility when energy intake is not tightly controlled.


Diabetes ◽  
1989 ◽  
Vol 38 (11) ◽  
pp. 1357-1364 ◽  
Author(s):  
J. Fowelin ◽  
S. Attvall ◽  
H. Von Schenck ◽  
U. Smith ◽  
I. Lager

Diabetes ◽  
1996 ◽  
Vol 45 (4) ◽  
pp. 415-421 ◽  
Author(s):  
M. Hettiarachchi ◽  
A. Watkinson ◽  
A. B. Jenkins ◽  
V. Theos ◽  
K. K. Ho ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 725
Author(s):  
Xiaoyun Song ◽  
Huijun Wang ◽  
Chang Su ◽  
Zhihong Wang ◽  
Feifei Huang ◽  
...  

Evidence shows time-of-day of energy intake are associated with health outcomes; however, studies of time-of-day energy patterns and their health implication are still lacking in the Asian population. This study aims to examine the time-of-day energy intake pattern of Chinese adults and to examine its associations with nutrient intakes, diet quality, and insulin resistance. Dietary data from three 24-h recalls collected during the 2015 China Health and Nutrition Survey (CHNS) were analyzed (n = 8726, aged ≥ 18 years). Time-of-day energy intake patterns were determined by latent class analysis (LCA). General Linear Models and Multilevel Mixed-effects Logistic Regression Models were applied to investigate the associations between latent time-of-day energy intake patterns, energy-adjusted nutrient intakes, diet quality score, and insulin resistance. Three time-of-day energy intake patterns were identified. Participants in the “Evening dominant pattern” were younger, had higher proportions of alcohol drinkers and current smokers. The “Evening dominant pattern” was associated with higher daily energy intake and a higher percentage of energy from fat (%) (p < 0.001), as well as higher insulin resistance risk (OR = 1.21; 95% CI: 1.05, 1.40), after adjusting for multivariate covariates. The highest diet quality score was observed in participants with “Noon dominant pattern” (p < 0.001). A higher proportion of energy in the later of the day was associated with insulin resistance in free-living individuals.


Sign in / Sign up

Export Citation Format

Share Document