NCT03188835: GB7

Effects of Fructose/Glucose-rich Diet on Brown Fat in Healthy Subjects (GB7)

Completed NA Last updated 27 January 2025

What this trial tests

NA trial testing Diet in Type2 Diabetes in 15 participants. Completed in 30 April 2021.

Timeline

23 May 2017

Primary endpoint
17 December 2020

30 April 2021

Quick facts

Lead sponsor	Université de Sherbrooke
Phase	NA
Status	Completed
Study type	INTERVENTIONAL
Allocation	randomized
Design	parallel
Masking	double
Primary purpose	basic science
Enrollment	15
Start date	23 May 2017
Primary completion	17 December 2020
Estimated completion	30 April 2021
Sites	1 location across Canada

Drugs / interventions tested

• Diet
• cold exposure
• 18FDG
• 11C-acetate — full drug profile →
• [3-3H]-glucose
• [U-13C]-palmitate
• 2H-Glycerol
• MRI/MRS
• Electromyogram (EMG)
• DXA
• Indirect calorimetry

Conditions studied

• Type2 Diabetes — all drugs for Type2 Diabetes →

Sponsor

Université de Sherbrooke — full company profile →

Who can join

Adults 20 to 35, male only, with Type2 Diabetes. Patients with the condition only — healthy volunteers not accepted.

Sponsor's own description

Activating brown and beige adipose tissue (herein described as BAT) has been recently recognized as a potential means to increase energy expenditure and lower blood glucose, however, BAT activity appears to be reduced with obesity, aging or Type 2 Diabetes (T2D). BAT has the unique capability to burn large amounts of sugar and fat and effectively dissipate this energy as heat due to the expression of uncoupling protein 1 (UCP1) which is controlled by a thermogenic gene program of transcription factors, co-activators and protein kinases. Thus, enhancing the thermogenic gene program may be beneficial for treating obesity and T2D. Despite the importance of BAT in regulating metabolism our understanding of the factors which suppress its metabolic activity with obesity, aging and T2D are largely unknown. Recently, it was shown that peripheral serotonin, which is regulated by the tryptophan hydroxylase 1 (Tph1), is a negative regulator of BAT metabolic activity. In addition to serotonin, other studies have indicated that pro-inflammatory stimuli may also inhibit BAT metabolic activity. These data suggest that reduced activation of BAT may be due to increases in peripheral serotonin and inflammation. Importantly, the gut microbiome has recently been recognized as an important regulator of serotonin and inflammatory pathways suggesting the observed effects of the microbiome on obesity, T2D may be mediated in part through reductions in BAT activity.

One mechanism by which the environment may impact BAT activity and the thermogenic gene program over the last 3 decades involves changes in our food supply as result of changes in agricultural production (chlorpyrifos, glyphosphate) and the addition of food additives (fructose). These agents have been reported to alter inflammation, serotonin metabolism and the gut microbiome indicating a potential bimodal (direct and indirect via the microbiome) mechanism by which they may alter the thermogenic gene program and contribute to chronic metabolic disease. Thus, our overarching hypothesis is that environmental agents and additives related to food production may contribute to the reduced metabolic activity of BAT. The objective is to identify and characterize how food production agents and additives reduce the metabolic activity of BAT.

Publications & conference data

1 peer-reviewed publication reference this trial (live from Europe PMC):

1. High-fructose feeding suppresses cold-stimulated brown adipose tissue glucose uptake independently of changes in thermogenesis and the gut microbiome.
   Richard G, Blondin DP, Syed SA, Rossi L, et al · · 2022 · cited 23× · PMID 36130480 · DOI 10.1016/j.xcrm.2022.100742