scholarly journals The effects of two-week program of individually measured physical activity on insulin resistance in obese non-insulin-dependent diabetes mellitus

2003 ◽  
Vol 60 (6) ◽  
pp. 683-690
Author(s):  
Milica Cizmic ◽  
Mirjana Zivotic-Vanovic ◽  
Slobodan Zivanic ◽  
Radosav Dragojevic

It is well known that under the influence of regular, individually measured aerobic physical activity, it is possible to raise the biological efficiency of insulin by several mechanisms: by increasing the number of insulin receptors, their sensitivity and efficiency, as well as by increasing glucose transporters GLUT-4 on the level of cell membrane. The aim of this research was to examine whether decreased insulin resistance could be achieved under the influence of the program of individually measured aerobic physical activity in the 2-week period, in the obese type 2 diabetes patients with the increased aerobic capacity (VO2)max. In 10 type 2 diabetes patients 47.6 ? 4.6 years of age (group E), in the 14-days period, program of aerobic training was applied (10 sessions - 35 min session of walking on treadmill, intensity 60.8 ? 5.7% (VO2)max, frequency 5 times a week ), as well as 1 600 kcal diet. At the same time, other 10 type 2 diabetes patients 45.9 ? 5.5 years of age (group C) were on 1 600 kcal diet. Before and after this period the following was measured in both groups: insulin sensitivity (M/I) by the method of hyperinsulin euglycemic clamp, and (VO2)max by Astrand test on ergocycle. In contrast to the group C, in the second testing of E group subjects a significant increase was obtained in M/I (1.23 ? 0.78 vs. 2.42 ? 0.95 mg/kg/min/mU p<0.001, 96.75%) as well as the increase of (VO2)max (26.34 ? 4.26 vs. 29.16 ? 5.01 ml/kg/min p<0.05, 10.7%). The results had shown that 2-week program of aerobic training had had significant influence on the increased aerobic capacity and insulin sensitivity in the tested patients.

2014 ◽  
Author(s):  
◽  
Leryn J. Boyle

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Individuals with type 2 diabetes (T2D) have blunted femoral artery insulin mediated blood flow which is critical for the delivery and uptake of glucose into skeletal muscle. However, it is unclear in humans the precise mechanisms by which insulin resistance impairs insulin stimulated blood flow. Further, chronic physical inactivity is a powerful stimulus for reduced insulin sensitivity and vascular dysfunction; however, the effects of short term, modest reductions in physical activity are limited. Thus, we examined 1) if inactivity for 5 days would impair endothelial function in healthy individuals (study one) 2) if reducing whole body insulin sensitivity, via 5 days of inactivity, would impair the blood flow response to insulin stimulation in parallel with glycemic control (study two) and 3) phosphorylation of endothelial nitric oxide (eNOS) and endothelin-1 (ET-1) production to insulin stimulation would be decreased and increased, respectively, in insulin resistant individuals (study three). We demonstrated significant reductions in endothelial function with only 5 days of reduced daily steps while blood flow to glucose ingestion was unaltered. Further, in obese humans with type 2 diabetes it does not appear that that the reduction in blood flow to 1 hr of insulin stimulation is due to altered peNOS or ET-1. Collectively, these data suggest that reduced daily physical activity and chronic insulin resistance mediate negative impacts on vascular function and insulin stimulated blood flow and signaling.


Diabetologia ◽  
2020 ◽  
Author(s):  
Alexandre Houzelle ◽  
Johanna A. Jörgensen ◽  
Gert Schaart ◽  
Sabine Daemen ◽  
Nynke van Polanen ◽  
...  

Abstract Aims/hypothesis Mitochondria operate in networks, adapting to external stresses and changes in cellular metabolic demand and are subject to various quality control mechanisms. On the basis of these traits, we here hypothesise that the regulation of mitochondrial networks in skeletal muscle is hampered in humans with compromised oxidative capacity and insulin sensitivity. Methods In a cross-sectional design, we compared four groups of participants (selected from previous studies) ranging in aerobic capacity and insulin sensitivity, i.e. participants with type 2 diabetes (n = 11), obese participants without diabetes (n = 12), lean individuals (n = 10) and endurance-trained athletes (n = 12); basal, overnight fasted muscle biopsies were newly analysed for the current study and we compared the levels of essential mitochondrial dynamics and quality control regulatory proteins in skeletal muscle tissue. Results Type 2 diabetes patients and obese participants were older than lean participants and athletes (58.6 ± 4.0 and 56.7 ± 7.2 vs 21.8 ± 2.5 and 25.1 ± 4.3 years, p < 0.001, respectively) and displayed a higher BMI (32.4 ± 3.7 and 31.0 ± 3.7 vs 22.1 ± 1.8 and 21.0 ± 1.5 kg/m2, p < 0.001, respectively) than lean individuals and endurance-trained athletes. Fission protein 1 (FIS1) and optic atrophy protein 1 (OPA1) protein content was highest in muscle from athletes and lowest in participants with type 2 diabetes and obesity, respectively (FIS1: 1.86 ± 0.79 vs 0.79 ± 0.51 AU, p = 0.002; and OPA1: 1.55 ± 0.64 vs 0.76 ± 0.52 AU, p = 0.014), which coincided with mitochondrial network fragmentation in individuals with type 2 diabetes, as assessed by confocal microscopy in a subset of type 2 diabetes patients vs endurance-trained athletes (n = 6). Furthermore, lean individuals and athletes displayed a mitonuclear protein balance that was different from obese participants and those with type 2 diabetes. Mitonuclear protein balance also associated with heat shock protein 60 (HSP60) protein levels, which were higher in athletes when compared with participants with obesity (p = 0.048) and type 2 diabetes (p = 0.002), indicative for activation of the mitochondrial unfolded protein response. Finally, OPA1, FIS1 and HSP60 correlated positively with aerobic capacity (r = 0.48, p = 0.0001; r = 0.55, p < 0.001 and r = 0.61, p < 0.0001, respectively) and insulin sensitivity (r = 0.40, p = 0.008; r = 0.44, p = 0.003 and r = 0.48, p = 0.001, respectively). Conclusions/interpretation Collectively, our data suggest that mitochondrial dynamics and quality control in skeletal muscle are linked to oxidative capacity in humans, which may play a role in the maintenance of muscle insulin sensitivity. Clinical Trial registry numbers NCT00943059, NCT01298375 and NL1888


2007 ◽  
Vol 32 (3) ◽  
pp. 549-556 ◽  
Author(s):  
Alison Kirk ◽  
Pierpaolo De Feo

The evidence that physical activity is an effective therapeutic tool in the management of insulin resistance and type 2 diabetes is well documented. Limited research has addressed how best to promote and maintain physical activity in these individuals. This paper explores strategies to enhance compliance to physical activity for patients with insulin resistance. Several evidence-based guidelines and reviews recommend that physical activity interventions are based on a valid theoretical framework. However, there is no evidence-based consensus on the best theory or the combination of theories to use. Motivational tools such as pedometers, wearable sensors measuring energy expenditure, and point of choice prompts appear to be effective at stimulating short-term substantial increases in physical activity, but further strategies to maintain physical activity behaviour change are required. Physical activity consultation has demonstrated effective physical activity promotion over periods of up to 2 years in people with type 2 diabetes. Future research should identify the longer term effects of this intervention and the effectiveness of different methods of delivery. Overall, there needs to be a lot more focus on this area of research. Without this, the abundance of research investigating the effects of physical activity on people with insulin resistance and type 2 diabetes is essentially redundant.


2021 ◽  
pp. 43-47
Author(s):  
Liliia Mogylnytska

Cardiovascular disease is the leading cause of death in diabetes mellitus. Endothelial dysfunction is the first step in the development of atherosclerotic vascular lesions, which underlies cardiovascular pathology, and adhesion molecules secreted by the endothelium during inflammatory changes are involved in the progression of this lesion. The objective: the serum level of adhesive molecules (ІCAM-1, VCAM-1, Е-selectin) in hypertensive and non-hypertensive type 2 diabetes patients as a marker of endothelial dysfunction and its relationship with other risk factors for cardiovascular disease was studied. Materials and methods. We examined 64 patients with type 2 diabetes, which were divided into two subgroups: the first subgroup – 41 hypertensive type 2 diabetes patients (age – 53,56±7,14 years, BMI – 32,2±87,4; HbA1c – 9,97±2,02%), the second subgroup – 23 nonhypertensive type 2 diabetes patients (age – 50,5±4,92 years, BMI – 25,4±5,22; HbA1c – 9,09±1,95%). The control group included 18 people without diabetes with normal blood pressure (age – 50,72±6,98 years, BMI – 24,71±4,88; HbA1c – 5,26±0,42%). The serum level was determined by immunoenzyme assay. The significance of the difference between the mean values was determined by the t-Student test. Multifactor regression analysis was used to assess the relationships between the studied factors. Results. We revealed an increase of serum levels of ІCAM-1, VCAM-1, Е-selectin in hypertensive (+71,62%, +68,42%, +66,95%, respectively) and non-hypertensive type 2 diabetes patients (+46,17%, +62,79%, +42,85%, respectively) compared with the control group (p<0,01). The serum concentration of ІCAM-1, Е-selectin was higher in hypertensive type 2 diabetes patients compared to non-hypertensive type 2 diabetes patients (+17,27%, +16,86%, respectively, p<0,01). There was a significant effect of Hb1Ac, lipids, insulin resistance on the serum level of ІCAM-1, VCAM-1, Е-selectin (p<0,01). The corresponding regression equations are derived. Conclusion. There is an increase of serum level of ІCAM-1, VCAM-1, Е-selectin in hypertensive and non-hypertensive type 2 diabetes patients, which indicates the development of endothelial dysfunction. Hypertension, hyperglycemia, dyslipidemia and insulin resistance contribute to the development of these changes.


2016 ◽  
Vol 85 (2) ◽  
pp. 26-28
Author(s):  
Andrew D Hanna ◽  
Natalie V Scime

Global rates of type 2 diabetes (T2D) among children and adolescents are steadily rising. As such, an increasing amount of attention and research has begun to focus on strategies to prevent this chronic and burdensome disease in pediatric populations. The purpose of this article is to briefly review current evidence pertaining to the effectiveness of physical activity versus metformin in improving insulin sensitivity of children at-risk (ie, obese and/or insulin resistant) for developing T2D. Potential barriers to each preventative intervention will also be discussed. Physical activity, both aerobic and resistance, has demonstrated effectiveness in a moderate number of demographically diverse pediatric studies. However, the pediatric population is already alarmingly sedentary with barriers such as lack of motivation, social stigma and discomfort presenting a challenge. A small number of studies have demonstrated the beneficial effects of metformin in children and adolescents for improved insulin sensitivity. However, longer and larger studies are required to confirm these findings and elucidate upon the long-term safety and efficacy of this pharmaceutical in pediatric populations. While no head-to-head studies examining physical activity and metformin exist in pediatric populations and more research is needed, current evidence seems to favour the use of physical activity given the larger quantity of studies and generalizability of its beneficial effects. Thus, physical activity should be emphasized in clinical and public health practice when targeting at-risk children and adolescents to prevent a T2D diagnosis.


Healthcare ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1010
Author(s):  
Wei-Hao Hsu ◽  
Chin-Wei Tseng ◽  
Yu-Ting Huang ◽  
Ching-Chao Liang ◽  
Mei-Yueh Lee ◽  
...  

Prediabetes should be viewed as an increased risk for diabetes and cardiovascular disease. In this study, we investigated its prevalence among the relatives and spouses of patients with type 2 diabetes or risk factors for prediabetes, insulin resistance, and β-cell function. A total of 175 individuals were included and stratified into three groups: controls, and relatives and spouses of type 2 diabetic patients. We compared clinical characteristics consisting of a homeostatic model assessment for insulin resistance (HOMA-IR) and beta cell function (HOMA-β), a quantitative insulin sensitivity check index (QUICKI), and triglyceride glucose (TyG) index. After a multivariable linear regression analysis, the relative group was independently correlated with high fasting glucose, a high TyG index, and low β-cell function; the relatives and spouses were independently associated with a low QUICKI. The relatives and spouses equally had a higher prevalence of prediabetes. These study also indicated that the relatives had multiple factors predicting the development of diabetes mellitus, and that the spouses may share a number of common environmental factors associated with low insulin sensitivity.


2021 ◽  
Author(s):  
Yu-Hua Tseng ◽  
Lee-Ming Chuang ◽  
Yi-Cheng Chang ◽  
Meng-Lun Hsieh ◽  
Lun Tsou ◽  
...  

Abstract Insulin resistance and obesity are pivotal features of type 2 diabetes mellitus. Peroxisome proliferator-activated receptor γ (PPARγ) is a master transcriptional regulator of systemic insulin sensitivity and energy balance. The anti-diabetic drug thiazolidinediones are potent synthetic PPARγ ligands and insulin sensitizers with undesirable side effects including increased adiposity, fluid retention, and osteoporosis, which limit their clinical use. We and others have proved that 15-keto-PGE2 is an endogenous natural PPARγ ligand. 15-keto-PGE2 is catalyzed by prostaglandin reductase 2 (PTGR2) to become inactive metabolites. We found that 15-keto-PGE2 level is increased in Ptgr2 knockout mice. Ptgr2 knockout mice were protected from diet-induced obesity, insulin resistance, and hepatic steatosis without fluid retention nor reduced bone mineral density. Diet-induced obese mice have drastically reduced 15-keto-PGE2 levels compared to lean mice. Administration of 15-keto-PGE2 markedly improved insulin sensitivity and prevented diet-induced obesity in mice. We demonstrated that 15-keto-PGE2 activates PPARγ through covalent binding to its cysteine 285 residue at helix 3, which restrained its binding pocket between helix 3 and β-sheets of the PPARγ ligand binding domain. This binding mode differs from the helix12-dependent binding mode of thiazolidinediones. We further identified a small-molecule PTGR2 inhibitor BPRPT245, which interferes the interaction between the substrate-binding sites of PTGR2 and 15-keto-PGE2. BPRPT245 increased 15-keto-PGE2 concentration, activated PPARγ, and promoted glucose uptake in adipocytes. BPRPT245 also prevented diet-induced obesity, improved insulin sensitivity and glucose tolerance, lowers fasting glucose without fluid retention and osteoporosis. In humans, reduced serum 15-keto-PGE2 levels were observed in patients with type 2 diabetes compared with controls. Furthermore, serum 15-keto-PGE2 levels correlate inversely with insulin resistance and fasting glucose in non-diabetic humans. In conclusion, we identified a new therapeutic approach to improve insulin sensitivity and protect diet-induced obesity through increasing endogenous natural PPARγ ligands without side effects of thiazolidinediones.


Author(s):  
Laura Stirane ◽  
Karlis Stirans ◽  
Leonora Pahirko ◽  
Janis Mednieks ◽  
Jelizaveta Sokolovska

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