Patients projected to have increase in body mass index also likely to develop increased plasma glucose levels and have diminished insulin response.
Insulin secretion and sensitivity improve proportionally with the loss of adipose tissue, or weight of an individual. Similarly, weight gain is accompanied by insulin resistance along with amplified plasma glucose levels. Both current and former weight have an effect on insulin and glucose metabolism, which are mutually exclusive. This relationship is best described when comparing two individuals who weigh exactly the same; if one of the individuals has recently lost a substantial amount of weight, he is expected to have a higher insulin resistance when matched to the other individual whose lower weight stayed fixed. Likewise, even higher insulin resistance is expected in a third individual who is obese and who does not lose a substantial amount of weight. Do these same rules of thumb apply to BMI fluctuations as well? The study presented in this article sought to clarify a relationship between individual’s blood glucose, insulin sensitivity, insulin resistance, and pancreatic beta cell function when compared to BMI changes over a period of 12 years.
This longitudinal, cohort trial enrolled community-living subjects from Personality and Total Health Through Life (PATH) study, a study that investigated health, cognition, and ageing. Subjects who were between the ages of 40 and 45, and 60 and 65 were taken into consideration to be enrolled; those who had a successful insulin extraction from blood, and those with documented BMI records were enrolled. Exclusion criteria were as follows: history of dementia, MMSE score of less than 26, or diagnosis of type 2 diabetes throughout the extent of the study. Two cohorts were created based on subject age – the 40s cohort and the 60s cohort. The cohorts were furthermore divided based on the BMI of the subjects: constant normal, constant high, increased, and decreased BMI trajectory. Constant normal trajectory was used as the reference group.
Baseline BMI was 25.51 kg/m2 in constant normal trajectory in the 40s cohort; constant high, increased, and decreased trajectory had baseline BMI of 37.17 kg/m2, 24.86 kg/m2, and 32.96 kg/m2, respectively. Change in BMI at the last follow-up was present across the groups. Constant normal, constant high, and increased trajectory BMI were found to be amplified (p<0.001 for all the groups) while decreased trajectory BMI was reduced at the completion of study (p<0.001). Furthermore, higher plasma insulin levels by 107%, greater insulin resistance by 105%, and increased beta cell function by 28% was seen with constant high trajectory when compared to the reference group. The decreased trajectory group was not associated with better outcomes. The group of subjects who were in the increased trajectory group had a statistically significant increase in plasma insulin, insulin resistance, and beta cell function by 76%, 79%, and 21%, respectively.
Subjects in the constant normal 60s cohort had a baseline BMI of 24.91 kg/m2. At the completion of the study, their BMI was found to be unchanged with a p-value of 0.89. A similar pattern was seen with constant high trajectory as well, p-value of 0.80. Subjects in the decreased trajectory group had a statistically significant reduction of their BMI, 25.44 kg/m2 at baseline versus 30.67 kg/m2 at the conclusion of the study. Increased trajectory subjects inversely reciprocated results were seen with decreased trajectory, their baseline BMI of 34.51 kg/m2 was increased to 43.78 kg/m2. Subjects in the constant high cohort had a statistically significant risk of having higher plasma insulin levels and insulin resistance when compared to the control group subjects. Subjects in the increased trajectory cohort had 77% more plasma insulin, 39% greater insulin resistance, and 13.5% higher beta cell function than their constant normal cohort counterparts. As it was seen in the 40s cohort, the decreased trajectory cohort was not associated with better outcomes when compared to the control group.
In conclusion, this study has determined that an individual’s blood glucose levels, insulin sensitivity, and beta cell function is contingent upon both the previous and present BMI measures. This effect was proven to be statistically significant. Although BMI may correspond to obesity, it does not take into consideration the percentage of body fat or muscle a person has. In fact, patients with a higher muscle mass will have a higher BMI as well, and not be considered obese due to their body fat percentage. Future studies that look into body fat mass and its effect on insulin sensitivity and secretion are warranted.
- Higher than normal BMI leads to diminished insulin sensitivity and increased plasma glucose levels in most people.
- Decreasing the BMI alone is not sufficient to increase insulin secretion and sensitivity.
- Both current and past BMI influence blood glucose levels, insulin sensitivity, and beta cell function.
Walsh EI, Shaw J, Cherbuin N. “Trajectories of BMI change impact glucose and insulin metabolism”. Nutrition, Metabolism and Cardiovascular Diseases. Jan 2018. www.nmcd-journal.com/article/S0939-4753(17)30314-9/pdf. Accessed on Jan 2018.
Kaarin Anstey, Helen Christensen, Peter Butterworth, et al. “388 Cohort Profile: The PATH through life project.” International Journal of Epidemiology. Aug. 2012. https://academic.oup.com/ije/article/41/4/951/683439. Accessed Jan. 2018.
Lamija Zimic, PharmD(c), University of South Florida, College of Pharmacy