Frequency of Interruptions to Sitting Time: Benefits for Postprandial Metabolism in Type 2 Diabetes
Ashleigh R. HomerFrances C. TaylorPaddy C. DempseyMichael J. WheelerParneet SethiMelanie K. TownsendMegan S. GraceDaniel J. GreenNeale CohenRobyn N. LarsenBronwyn A. KingwellNeville OwenDavid W. Dunstan
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<b>Purpose:</b> To determine whether interrupting sitting with brief bouts of simple resistance activities (SRAs) at different frequencies improves postprandial glucose, insulin and triglycerides in adults with medication-controlled type 2 diabetes (T2D). <p><b>Methods:</b> Participants [n=23, 10 females, Age: 62±8 y (mean±SD), BMI: 32.7 ± 3.5 kg<sup>.</sup>m<sup>-2</sup>] completed a three-armed randomized crossover trial (6-14 day washout): sitting uninterrupted for 7 h (SIT); sitting with 3-minute SRAs (half-squats, calf raises, gluteal contractions, and knee raises) every 30 minutes (SRA3); and, sitting with 6-minute SRAs every 60 minutes (SRA6). Net incremental areas under the curve (iAUC<sub>net</sub>) for glucose, insulin, and triglycerides were compared between conditions.</p> <p><b>Results:</b> <a>Glucose and insulin 7 h iAUC<sub>net </sub>were attenuated significantly during SRA6 (glucose 17.0 mmol<sup>.</sup>h<sup>.</sup>L<sup>-1</sup>, 95% CI 12.5, 21.4; insulin 1229 pmol<sup>.</sup>h<sup>.</sup>L<sup>-1</sup>, 95% CI 982, 1538) when compared to SIT (glucose 21.4 mmol<sup>.</sup>h<sup>.</sup>L<sup>-1</sup>, 95% CI 16.9, 25.8; insulin 1411 pmol<sup>.</sup>h<sup>.</sup>L<sup>-1</sup>, 95% CI 1128, 1767; <i>P</i> < 0.05), and compared to SRA3 ( for glucose only; 22.1 mmol<sup>.</sup>h<sup>.</sup>L<sup>-1</sup>, 95% CI 17.7, 26.6; <i>P </i>= 0.01) No significant differences in glucose or insulin iAUC<sub>net</sub> were observed comparing SRA3 and SIT. There was no statistically significant effect of condition on triglyceride iAUC<sub>net</sub>. </a></p> <p><b>Conclusion:</b> In adults with medication-controlled T2D, interrupting prolonged sitting with 6-minute SRAs every 60 minutes reduced postprandial glucose and insulin responses. Other frequencies of interruptions and potential longer-term benefits require examination to clarify clinical relevance. </p>Cite
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Nonalcoholic fatty liver disease (NAFLD), hepatic insulin resistance, and type 2 diabetes are all strongly associated and are all reaching epidemic proportions. Whether there is a causal link between NAFLD and hepatic insulin resistance is controversial. This review will discuss recent studies in both humans and animal models of NAFLD that have implicated increases in hepatic diacylglycerol (DAG) content leading to activation of novel protein kinase Cϵ (PKCϵ) resulting in decreased insulin signaling in the pathogenesis of NAFLD-associated hepatic insulin resistance and type 2 diabetes. The DAG-PKCϵ hypothesis can explain the occurrence of hepatic insulin resistance observed in most cases of NAFLD associated with obesity, lipodystrophy, and type 2 diabetes.
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Objective To investigate the relationship between postprandial blood lipid,serum insulin and blood glucose in the patients with type 2 diabetes (DM2).Methods 60 patients with DM2 were studied and their fasting and postprandial levels of blood lipid,apolipoprotein(Apo),serum insulin(Ins),plasma glucose(PG) were measured.Results (1)The levels of fasting and postprandial PG,Ins,TG were significantly increased and HDL and ApoA 1/ApoB 100 remarkably decreased, being compared with normal controls (P0.05);(2)Postprandial TG、LDL were positively correlated with fasting Ins (P0.05),Postprandial TC was positively correlated with postprandial PG (P0.05).Conclusion Patients with DM2 have significant disorder of postprandial blood lipid and lipoprotein metabolism, being remarkably correlated with the levels of postprandial PG and fasting Ins.
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Postprandial hyperlipemia produces long-term derangements in lipid/lipoprotein metabolism, vascular endothelial dysfunction, hypercoagulability, and sympathetic hyperactivity which are strongly linked to atherogenesis. The purpose of this review is to (1) provide a qualitative analysis of the available literature examining the dysregulation of postprandial lipid metabolism in the presence of obesity, (2) inspect the role of adiposity distribution and sex on postprandial lipid metabolism, and (3) examine the role of energy deficit (exercise- and/or energy restriction-mediated), isoenergetic low-carbohydrate diets, and omega-3 (n-3) fatty acid supplementation on postprandial lipid metabolism. We conclude from the literature that central adiposity primarily accounts for sex-related differences in postprandial lipemia and that aerobic exercise attenuates this response in obese or lean men and women to a similar extent through potentially unique mechanisms. In contrast, energy restriction produces only mild reductions in postprandial lipemia suggesting that exercise may be superior to energy restriction alone as a strategy for lowering postprandial lipemia. However, isoenergetic very low-carbohydrate diets and n-3 fatty acid supplementation reduce postprandial lipemia indicating that macronutrient manipulations reduce postprandial lipemia in the absence of energy restriction. Therefore, interactions between exercise/energy restriction and alterations in macronutrient content remain top priorities for the field to identify optimal behavioral treatments to reduce postprandial lipemia.
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Chronic hyperglycaemia, confirmed with HbA1c levels, is a leading cause of diabetic complications. Recent studies point to a significant effect of postprandial glycaemia which results from an impaired ability of early secretion of insulin in type II diabetes. Postprandial hyperglycaemia is a frequent phenomenon in people with diabetes with satisfactory control of diabetes based on checks of HbA1c levels. Many authors demonstrate statistically more significant correlations between postprandial hyperglycaemia and HbA1c levels, compared to correlation of fasting glycaemia. Monitoring of postprandial glycaemia is a significant means for improving co-operation with a patient and provides a physician with a possibility of choice between an appropriate type of peroral antidiabetic or insulin.
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Objective To investigate the correlation of the elderly postprandial hypotension and vascular endothelial function.Methods 270 cases of elderly postprandial hypotension in elderly outpatients of our hospital were as experimental group,120 cases of healthy were as control group.Correlation of the elderly postprandial hypotension with von willebrand factor(vwF) and fibrinogen(Fbg) was analyzed.Results Hypotension after breakfast were 120 cases,105 cases were in postprandial hypotension,hypotension after dinner were of 45 cases,expression of vwF and Fbg in the experimental group compared with the control group,all had a significant difference(P 0.05).The expression of vwF and Fbg with postprandial hypotension had positive correlation(r = 0.589,0.603,P 0.05).Conclusion The expression of vwF and Fbg in the elderly postprandial were significantly increased,the elderly postprandial hypotension with vwF and Fbg have positive correlation.This can provide new methods and basis for the treatment of elderly postprandial hypotension.
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We thank Prof. Dogru and colleagues for their interest in our recent article on the importance of adipocyte fatty acid binding protein (AFABP) in nonalcoholic fatty liver disease (NAFLD).1 It is now well accepted that NAFLD is the hepatic manifestation of the metabolic syndrome and as such is intimately associated with insulin resistance, visceral obesity, and dyslipidemia.2 Insulin resistance, which is a key characteristic of both conditions, has also been associated with NAFLD progression from simple steatosis to nonalcoholic steatohepatitis.3 We used the homeostasis model assessment of insulin resistance (HOMA-IR) to reflect the spectrum of insulin sensitivity. This index has been shown to correlate with the results of euglycemic-hyperinsulinemic clamp in patients without diabetes and with type 2 diabetes, including those treated with metformin and other oral hypoglycemic agents.4, 5 We were careful to exclude those taking thiazolidenediones, which have been shown to significantly affect circulating adipokine levels,6, 7 in contrast to sulfonylureas and metformin, which have not.7, 8 Type 2 diabetes eventually ensues in many subjects with increasing insulin resistance and is associated with more progressive fatty liver disease9; therefore, we decided not to exclude subjects with type 2 diabetes in our study. Although we agree it would be interesting to further subclassify subjects by glucose dysregulation status, the use of post hoc subset analysis is far less robust statistically and prone to type 2 error. We agree that metabolic variables and, in particular, measures of insulin resistance are important to consider when interpreting data on adipocytokines, which are intimately related to these factors. Indeed, our data showed the close association between both AFABP and lipocalin-2 to insulin resistance, body mass index, and waist circumference. To ensure our findings were independent of key confounders, we performed multivariate analysis for each histological endpoint in NAFLD using those factors significant on univariate analysis.1 We demonstrated that the association between AFABP and necroinflammatory and fibrotic activity is independent of abdominal obesity (the waist-hip ratio), cholesterol, high-density lipoprotein, and insulin resistance. For further clarity, as suggested by Prof. Dogru, we provide in Table 1 the relationship between AFABP and disease severity in NAFLD, directly controlled for insulin resistance and the key metabolic variables of body mass index, low-density lipoprotein, high-density lipoprotein, triglycerides, and glucose. This conclusively demonstrates that AFABP plays an important role in the pathogenesis of NAFLD independent of metabolic confounders. David van der Poorten*, Kerry-Lee Milner , Donald J. Chisholm , Jacob George*, * Storr Liver Unit, Westmead Millennium Institute, University of Sydney, Sydney, Australia, Garvan Institute of Medical Research, University of New South Wales, Sydney, Australia.
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