Key result
In a rat model of type 1 diabetes, the β3-adrenoceptor agonist CL316,243 increased interscapular brown adipose tissue metabolic activity up to threefold compared to saline.
Why the study?
Does the β3-adrenoceptor agonist CL316,243 or NET blocker atomoxetine improve [(18)F]FDG metabolic activity in interscapular brown adipose tissue in a streptozotocin-induced type 1 diabetes rat model?
Does the β3-adrenoceptor agonist CL316,243 or NET blocker atomoxetine improve [(18)F]FDG metabolic activity in interscapular brown adipose tissue in a streptozotocin-induced type 1 diabetes rat model?
β3-adrenoceptor agonists can increase brown adipose tissue metabolic activity in a type 1 diabetes rat model, suggesting a potential role in modulating blood sugar levels.
Answers are grounded in this paper and cite their sources.
BAT activation remains measurable in T1DM rat models; hypothesis-generating for metabolic therapies but leaves open human translation.
Metabolic activity of brown adipose tissue (BAT) is activated by β3-adrenoceptor agonists and norepinephrine transporter (NET) blockers and is measurable using [(18)F]fluorodeoxyglucose ([(18)F]FDG) positron emission tomography/computed tomography (PET/CT) in rats. Using the streptozotocin (STZ)-treated rat model of type 1 diabetes mellitus (T1DM), we investigated BAT activity in this rat model under fasting and nonfasting conditions using [(18)F]FDG PET/CT. Drugs that enhance BAT activity may have a potential for therapeutic development in lowering blood sugar in insulin-resistant diabetes. Rats were rendered diabetic by administration of STZ and confirmed by glucose measures. [(18)F]FDG was injected in the rats (fasted or nonfasted) pretreated with either saline or β3-adrenoceptor agonist CL316,243 or the NET blocker atomoxetine for PET/CT scans. [(18)F]FDG metabolic activity was computed as standard uptake values (SUVs) in interscapular brown adipose tissue (IBAT) and compared across the different drug treatment conditions. Blood glucose levels > 500 mg/dL were established for the STZ-treated diabetic rats. Under fasting conditions, average uptake of [(18)F]FDG in the IBAT of STZ-treated diabetic rats was approximately 70% lower compared to that of normal rats. Both CL316,243 and atomoxetine activated IBAT in normal rats had an SUV > 5, whereas activation in STZ-treated rats was significantly lower. The agonist CL316,243 activated IBAT up to threefold compared to saline in the fasted STZ-treated rat. In the nonfasted rat, the IBAT activation was up by twofold by CL316243. Atomoxetine had a greater effect on lowering blood sugar levels compared to CL316,243 in the nonfasted rats. A significant reduction in metabolic activity was observed in the STZ-treated diabetic rodent model. Increased IBAT activity in the STZ-treated diabetic rat under nonfasted conditions using the β3-adrenoceptor agonist CL316,243 suggests a potential role of BAT in modulating blood sugar levels. Further studies are needed to evaluate the therapeutic role of β3-adrenoceptor agonists in insulin-resistant T1DM.
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Baranwal et al. (2015) studied Streptozotocin-induced type 1 diabetes. CL316,243 or atomoxetine vs. Saline was evaluated on [(18)F]FDG metabolic activity (standard uptake values) in interscapular brown adipose tissue. In a rat model of type 1 diabetes, the β3-adrenoceptor agonist CL316,243 increased interscapular brown adipose tissue metabolic activity up to threefold compared to saline.
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