Evidence for fatty acids mediating CL 316,243-induced reductions in blood glucose in mice

MacPherson, Rebecca E. K.; Castellani, L; Beaudoin, Marie-Soleil; Wright, David C.

doi:10.1152/ajpendo.00287.2014

Cited by 36 publications

(48 citation statements)

References 36 publications

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“…In the present study, where beta adrenergic stimulation is being exogenously provided, this potential confounding issue would likely be avoided. In fact, we have previously shown that CL-mediated increases in plasma glycerol and fatty acid release are intact in IL-6 À/À mice suggesting that beta adrenergic signaling in adipose tissue is normal in these animals (MacPherson et al 2014).…”

Section: Discussionmentioning

confidence: 96%

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The contribution of IL-6 to beta 3 adrenergic receptor mediated adipose tissue remodeling

et al. 2015

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The chronic activation of beta 3 adrenergic receptors results in marked alterations in adipose tissue morphology and metabolism, including increases in mitochondrial content and the expression of enzymes involved in lipogenesis and glyceroneogenesis. Acute treatment with CL 316,243, a beta 3 adrenergic agonist, induces the expression of interleukin 6. Interestingly, IL-6 has been shown to induce mitochondrial genes in cultured adipocytes. Therefore, the purpose of this paper was to examine the role of interleukin 6 in mediating the in vivo effects of CL 316,243 in white adipose tissue. Circulating IL-6, and markers of IL-6 signaling in white adipose tissue were increased 4 h following a single injection of CL 316,243 in C57BL6/J mice. Once daily injections of CL 316,243 for 5 days increased the protein content of a number of mitochondrial proteins including CORE1, Cytochrome C, PDH, MCAD, and Citrate Synthase to a similar extent in adipose tissue from WT and IL-6−/− mice. Conversely, CL 316,243-induced increases in COXIV and phosphorylated AMPK were attenuated in IL-6−/− mice. Likewise, the slight, but significant, CL 316,243-induced increases in ATGL, PEPCK, and PPARγ, were reduced or absent in adipose tissue IL-6−/− mice. The attenuated response to CL 316,243 in white adipose tissue in IL-6−/− mice was associated with reductions in whole-body oxygen consumption and energy expenditure in the light phase. Our findings suggest that IL-6 plays a limited role in CL 316,243-mediated adipose tissue remodeling.

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Section: Discussionmentioning

confidence: 96%

“…In fact, we have previously shown that CL‐mediated increases in plasma glycerol and fatty acid release are intact in IL‐6 −/− mice suggesting that beta adrenergic signaling in adipose tissue is normal in these animals (MacPherson et al. ).…”

Section: Discussionmentioning

confidence: 99%

The contribution of IL-6 to beta 3 adrenergic receptor mediated adipose tissue remodeling

et al. 2015

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“…; MacPherson et al . ), serum non‐esterified fatty acids (NEFA) and glycerol concentrations were determined on a 96‐well plate measured using commercially available kits (NEFA: Wako Diagnostics, Richmond, VA; Glycerol: Sigma‐Aldrich, Oakville, ON, Canada). Serum creatine kinase was measured using a kit from Pointe Scientific (Canton, MI, USA).…”

Section: Methodsmentioning

confidence: 99%

Prior exercise training improves cold tolerance independent of indices associated with non‐shivering thermogenesis

Knuth

Peppler

Townsend

et al. 2018

The Journal of Physiology

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Shivering is one of the first defences against cold, and as skeletal muscle fatigues there is an increased reliance on non-shivering thermogenesis. Brown and beige adipose tissues are the primary thermogenic tissues regulating this process. Exercise has also been shown to increase the thermogenic capacity of subcutaneous white adipose tissue. Whether exercise has an effect on the adaptations to cold stress within adipose tissue and skeletal muscle remains to be shown. Male C57BL/6 mice were either subjected to voluntary wheel running or remained sedentary for 12 days. Exercise led to decreased body weight and increased glucose tolerance. Mice were then divided into groups kept at 25°C room temperature or a cold challenge of 4°C for 48 h. Exercised mice were protected against cold-induced reductions in weight and in parallel with increased food intake. Providing exercised mice with the same amount of food as sedentary mice eliminated the protection against cold-induced weight loss. Cold exposure led to greater reductions in rectal temperature in sedentary compared to exercised mice. This protective effect was not explained by differences in the browning of white adipose tissue or brown adipose tissue mass. Similarly, the ability of the β -adrenergic agonist CL 316,243 to increase energy expenditure was attenuated in previously exercised mice, suggesting that the activation of uncoupling protein-1 in brown and/or beige adipocytes is not the source of protective effects. We speculate that the protection against cold-induced reductions in rectal temperature could potentially be linked to exercise-induced alterations in skeletal muscle.

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“…Nonesterified fatty acids (NEFA; Wako Diagnostics) and glycerol (cat no. F6428; Sigma Aldrich) were measured on a 96well plate as previously described (MacPherson, Castellani, Beaudoin, & Wright, 2014). Glucagon and insulin were measured via enzyme-linked immunosorbent assays (ELISA) (cat no.…”

Section: Serum Measurementsmentioning

confidence: 99%

Epinephrine responsiveness is reduced in livers from trained mice

et al. 2020

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The liver is the primary metabolic organ involved in the endogenous production of glucose through glycogenolysis and gluconeogenesis. Hepatic glucose production (HGP) is increased via neural‐hormonal mechanisms such as increases in catecholamines. To date, the effects of prior exercise training on the hepatic response to epinephrine have not been fully elucidated. To examine the role of epinephrine signaling on indices of HGP in trained mice, male C57BL/6 mice were either subjected to 12 days of voluntary wheel running or remained sedentary. Epinephrine, or vehicle control, was injected intraperitoneally on day 12 prior to sacrifice with blood glucose being measured 15 min postinjection. Epinephrine caused a larger glucose response in sedentary mice and this was paralleled by a greater reduction in liver glycogen in sedentary compared to trained mice. There was a main effect of epinephrine to increase the phosphorylation of protein kinase‐A (p‐PKA) substrates in the liver, which was driven by increases in the sedentary, but not trained, mice. Similarly, epinephrine‐induced increases in the mRNA expression of hepatic adrenergic receptors (Adra1/2a, Adrb1), and glucose‐6‐phosphatase (G6pc) were greater in sedentary compared to trained mice. The mRNA expression of cAMP‐degrading enzymes phosphodiesterase 3B and 4B (Pde3b, Pde4b) was greater in trained compared to sedentary mice. Taken together, our data suggest that prior exercise training reduces the liver's response to epinephrine. This could be beneficial in the context of training‐induced glycogen sparing during exercise.

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Evidence for fatty acids mediating CL 316,243-induced reductions in blood glucose in mice

Cited by 36 publications

References 36 publications

The contribution of IL-6 to beta 3 adrenergic receptor mediated adipose tissue remodeling

The contribution of IL-6 to beta 3 adrenergic receptor mediated adipose tissue remodeling

Prior exercise training improves cold tolerance independent of indices associated with non‐shivering thermogenesis

Epinephrine responsiveness is reduced in livers from trained mice

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