Dutta, Nirjhar

Background Sedentary time has been shown to have deleterious effects on health. Today's workforce spends most of the day sitting. The objective of this study was to evaluate the effect of workplace interventions to decrease sedentary time on cardiometabolic risk factors. Methods Sedentary office workers (n=127; ages 22‐64; BMI=28.5±6.1 kg/m 2 ) were recruited from three Minnesota employers and randomized to one of four intervention groups for 6 months: 1) Control, 2) Move (蠅30 min of light activity during the workday), 3) Stand (standing 蠅50% of the workday using a sit‐stand workstation), or 4) Stand+Move (combined Stand and Move). A 'metabolic risk score' (MRS) was calculated at baseline and 6 months using the following cardiometabolic risk factors: blood pressure, fasting blood glucose, log of fasting triglycerides, and HDL‐cholesterol. A z‐score was computed for each risk factor for each subject [(subject value – sample mean)/sample SD]. The MRS was derived by summing the z‐scores (HDL‐z subtracted). Results There was a significant intervention effect on MRS (p<.01). A seasonal time trend was observed, with MRS increasing significantly in Control and Move groups (p<.001), but not for the Stand and Stand+Move. Results (mean±se) are shown in Figure 1. Conclusions Sit‐stand workstations combined with an intervention to increase light physical activity at work may be an effective tool to improve cardiometabolic risk. image

Objective: This study was conducted to determine whether installation of sit-stand desks (SSDs) could lead to decreased sitting time during the workday among sedentary office workers. Methods: A randomized cross-over trial was conducted from January to April, 2012 at a business in Minneapolis. 28 (nine men, 26 full-time) sedentary office workers took part in a 4 week intervention period which included the use of SSDs to gradually replace 50% of sitting time with standing during the workday. Physical activity was the primary outcome. Mood, energy level, fatigue, appetite, dietary intake, and productivity were explored as secondary outcomes. Results: The intervention reduced sitting time at work by 21% (95% CI 18%–25%) and sedentary time by 4.8 min/work-hr (95% CI 4.1–5.4 min/work-hr). For a 40 h work-week, this translates into replacement of 8 h of sitting time with standing and sedentary time being reduced by 3.2 h. Activity level during non-work hours did not change. The intervention also increased overall sense of well-being, energy, decreased fatigue, had no impact on productivity, and reduced appetite and dietary intake. The workstations were popular with the participants. Conclusion: The SSD intervention was successful in increasing work-time activity level, without changing activity level during non-work hours.

Diabetic gastroparesis is associated with increased oxidative stress attributable to loss of upregulation of heme oxygenase-1 (HO1), with resultant damage to interstitial cells of Cajal and delayed gastric emptying. These changes can be reversed by induction of HO1. HO1 catalyzes the breakdown of heme into iron, biliverdin and, carbon monoxide (CO). The aim of this study was to determine whether inhalation of CO can mimic the protective effects of HO1. Nonobese diabetic (NOD) mice with delayed gastric emptying were treated with CO inhalation. Serum malondialdehyde was measured as a marker of oxidative stress. Gastric emptying of solids was measured using a [13C]octanoic acid breath test. Kit expression levels were determined in immunoblots of protein extracted from the external muscle layers of the gastric body and antrum. The effect of CO on oxidative stress and gastric emptying was also determined in the presence of HO activity inhibitor chromium mesoporphyrin. CO inhalation reduced oxidative stress, restored Kit expression and reversed delayed gastric emptying in diabetic NOD mice with delayed gastric emptying. CO inhalation maintained this effect in the presence of the HO activity inhibitor, chromium mesoporphyrin, also resulting in restoration of the delay in gastric emptying. CO inhalation mimics the protective effect of upregulation of HO1 and decreased oxidative stress, increased Kit expression, and restored delay in gastric emptying. This effect of CO was independent of HO activity, suggesting that its effects were downstream of HO1. CO represents a potential therapeutic option for treatment of diabetic gastroparesis.