The insulin therapy–mediated weight gain in patients with type 2 diabetes (T2D) may relate to altered physical activity patterns (1). In this study, we examined the hypothesis that initiation of insulin therapy would be associated with an increase in sedentary behavior (i.e., sitting time) and lower low-, moderate-, and vigorous-intensity physical activity, which would subsequently relate to weight gain.

We included 40 T2D patients who started insulin therapy and followed these patients for a period of 12 months. Patients were randomly selected from one university hospital, three nonuniversity teaching hospitals, and four primary care practices. The decision to start insulin treatment was at the discretion of the responsible physician and was always based on failure of glycemic control while on oral glucose-lowering agents and diet. Measurements were performed before and 6 months and 12 months after initiation of insulin therapy. We examined body weight, waist-to-hip circumference, fasting glucose, and HbA1c using standardized procedures. Free-living daytime physical activity was objectively measured (SenseWear Pro3 Armband, BodyMedia, Pittsburgh, PA) (2). We examined 1) time (hours/day) spent in sitting (<1.5 METs), low-intensity physical activity (LPA) (2.1–3.0 METs), and moderate- to vigorous-intensity physical activity (MVPA) (>3.0 METs); 2) steps per day; and 3) sit-to-stand maneuvers (transition from ≥5 min sitting to LPA). Results are expressed as mean ± SD.

Over 12 months, body weight increased 2.9 ± 4.5 kg (P < 0.05). This observation is largely in line with earlier findings (3). Furthermore, fasting glucose and HbA1c decreased over 12 months (both P < 0.05). Interestingly, we found an increase in sitting time and a decrease in LPA but no change in MVPA (Fig. 1A–C). Number of steps (7,854 ± 3,936 to 6,060 ± 3,022) and sit-to-stand maneuvers (20 ± 5 to 18 ± 6) significantly decreased (both P values <0.05). These findings show an increase in sedentary behavior rather than a decrease in physical activity (including exercise time) that occurs simultaneously with an increase in body weight after initiation of insulin therapy. Because sedentary behavior replaced LPA, lower energy expenditure may relate to our observation (4). However we found no relationship between changes in energy expenditure and weight gain (r = −0.195, P = 0.227). Excessive caloric intake is less likely to explain our observation, as food diaries revealed no increase in caloric intake (1,721 ± 839 to 1,460 ± 367 calories/day, P = 0.074).

Figure 1

AC: Physical activity patterns in T2D patients at baseline (T0) and after 6 months (T6) and 12 months (T12) of the start of insulin therapy, where patterns are presented as sitting (A), LPA (B), and MVPA (C). The plot elements are presented as follows: the length of the box represents the interquartile range (the distance between the 25th and the 75th percentiles), the horizontal line in the box interior represents the median, and the vertical lines issuing from the box extend to the minimum and maximum values of the variables. *Post hoc analysis significantly different from T0 at P < 0.05. D and E: Spearman correlations of change in sitting time between baseline and 12 months of insulin therapy and weight gain (D) and waist circumference (E) among T2D patients with baseline BMI <30 kg/m2. Spearman rank correlation coefficients (r) are shown for each correlation. Solid lines indicate linear regression function.

Figure 1

AC: Physical activity patterns in T2D patients at baseline (T0) and after 6 months (T6) and 12 months (T12) of the start of insulin therapy, where patterns are presented as sitting (A), LPA (B), and MVPA (C). The plot elements are presented as follows: the length of the box represents the interquartile range (the distance between the 25th and the 75th percentiles), the horizontal line in the box interior represents the median, and the vertical lines issuing from the box extend to the minimum and maximum values of the variables. *Post hoc analysis significantly different from T0 at P < 0.05. D and E: Spearman correlations of change in sitting time between baseline and 12 months of insulin therapy and weight gain (D) and waist circumference (E) among T2D patients with baseline BMI <30 kg/m2. Spearman rank correlation coefficients (r) are shown for each correlation. Solid lines indicate linear regression function.

Close modal

T2D patients with BMI <30 kg/m2 (aged 64 ± 10 years) showed less sitting time (P = 0.012) and more LPA (P = 0.012) than those with BMI ≥30 kg/m2 (aged 57 ± 9 years). Surprisingly, upon insulin therapy, BMI and waist circumference increased in subjects with BMI <30 kg/m2 but not in those with BMI ≥30 kg/m2. Similarly, patients with BMI <30 kg/m2 but not those with BMI ≥30 kg/m2 demonstrated an increase in sitting time and a decrease in energy expenditure and steps/day (data not shown). We found significant, positive relationships between changes in weight and waist circumference versus sitting time (Fig. 1D and E). This fits with previous work in populations without diabetes, where an increase in sedentary behavior was related to weight gain (5). T2D patients with BMI ≥30 kg/m2 did not demonstrate these relationships (r = −0.186 and −0.041, P = 0.474 and 0.879, for weight and waist circumference, respectively). A potential explanation for these unexpected between-group differences may relate to a ceiling effect in sedentary behavior in patients with BMI ≥30 kg/m2. Indeed, the average sitting time of 12.5 h makes it practically difficult to further increase sedentary behavior.

We observed that the initiation of insulin therapy was associated with an increase in sedentary behavior and limited changes in MVPA. This suggests that increased sedentary behavior, especially in nonobese T2D patients, may contribute to body weight gain after initiation of insulin therapy. These findings suggest that sedentary behavior assessment and intervention may be needed in T2D management.

Funding. This project is funded through a personal PhD-studentship Award for Y.A.W.H. from the Radboud University Medical Center.

Duality of Interest. No potential conflicts of interest relevant to this article were reported.

Author Contributions. Y.A.W.H. was responsible for data analysis, drafted the first manuscript, and performed and interpreted statistical analysis. H.J.J. contributed to data collection. M.T.E.H. performed and interpreted statistical analysis. C.J.T. devised and designed the experiment, arranged funding, and performed and interpreted statistical analysis. D.H.J.T. devised and designed the experiment, arranged funding, and performed and interpreted statistical analysis. All authors contributed to writing of the manuscript and provided approval of the final version. Y.A.W.H., H.J.J., M.T.E.H., C.J.T., and D.H.J.T. are the guarantors of this work and, as such, had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Prior Presentation. Parts of this study were presented at the American College of Sports Medicine 64th Annual Meeting, Denver, CO, 30 May–3 June 2017.

1.
Sternfeld
B
,
Wang
H
,
Quesenberry
CP
 Jr
, et al
.
Physical activity and changes in weight and waist circumference in midlife women: findings from the Study of Women’s Health Across the Nation
.
Am J Epidemiol
2004
;
160
:
912
922
2.
Brazeau
AS
,
Karelis
AD
,
Mignault
D
,
Lacroix
MJ
,
Prud'homme
D
,
Rabasa-Lhoret
R
.
Test-retest reliability of a portable monitor to assess energy expenditure
.
Appl Physiol Nutr Metab
2011
;
36
:
339
343
3.
Yadgar-Yalda
R
,
Colman
PG
,
Fourlanos
S
,
Wentworth
JM
.
Factors associated with insulin-induced weight gain in an Australian type 2 diabetes outpatient clinic
.
Intern Med J
2016
;
46
:
834
839
4.
Ryan
M
,
Livingstone
MB
,
Ducluzeau
PH
,
Sallé
A
,
Genaitay
M
,
Ritz
P
.
Is a failure to recognize an increase in food intake a key to understanding insulin-induced weight gain?
Diabetes Care
2008
;
31
:
448
450
5.
Thorp
AA
,
Owen
N
,
Neuhaus
M
,
Dunstan
DW
.
Sedentary behaviors and subsequent health outcomes in adults: a systematic review of longitudinal studies, 1996-2011
.
Am J Prev Med
2011
;
41
:
207
215
Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at http://www.diabetesjournals.org/content/license.