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Three types of adipocytes, white, brown, and beige, regulate the systemic energy balance through the storage and expenditure of chemical energy. In addition, adipocytes produce various bioactive molecules known as adipokines. In contrast to white adipocyte‐derived molecules, less information is available on the adipokines produced by brown adipocytes (batokine). This study explored the regulatory expression of interleukin (IL)‐6 in cell culture studies. Norepinephrine or a nonselective β‐adrenergic receptor agonist increased the expression of IL‐6 in primary brown adipocytes and HB2 brown adipocytes. Treatment with forskolin (Fsk), an activator of the cAMP‐dependent protein kinase (PKA) pathway (downstream signaling of the β‐adrenergic receptor), efficiently stimulated IL‐6 expression in brown adipocytes and myotubes. Phosphorylated CREB and phosphorylated p38 MAP kinase levels were increased in Fsk‐treated brown adipocytes within 5 min. In contrast, a long‐term (∼60 min and ∼4 h) treatment with Fsk was required for increase in STAT3 phosphorylation and C/EBPβ expression, respectively. The PKA, p38 MAP kinase, STAT3, and C/EBPβ pathways are required for the maximal IL‐6 expression induced by Fsk, which were verified by use of various inhibitors of these signal pathways. Vitamin C enhanced Fsk‐induced IL‐6 expression through the extracellular signal‐regulated kinase activity. The present study provides basic information on the regulatory expression of IL‐6 in activated brown adipocytes. Significance statement: White adipocytes accumulate excess energy as fat, whereas brown adipocytes consume the chemical energy of fat and carbohydrates as heat. Adipocytes also secrete bioactive molecules called adipokine. Interleukin‐6 (IL‐6) is produced not only in white adipocytes but also brown adipocytes, but the regulation of IL‐6 expression in brown adipocytes is unclear. We explored the mechanisms underlying IL‐6 gene induction in activated brown adipocytes. Forskolin increased IL‐6 expression in brown adipocytes through stimulated phosphorylation of CREB, p38 MAP kinase, and STAT3. In addition, C/EBPβ induction was required for the enhancement of IL‐6 induction. Vitamin C also promoted forskolin‐induced IL‐6 expression. The present study provides basic information on the regulatory expression of IL‐6 in activated brown adipocytes. [ABSTRACT FROM AUTHOR]

BACKGROUND Magnesium (Mg) is highly bioavailable in kombu compared with other edible seaweeds. However, a considerable amount of Mg is lost during industrial processing and cooking of kombu. We hypothesized that thinly shaved kombu (TSK), a traditional Japanese kombu product, is a suitable Mg source for daily diets because TSK hardly loses Mg during processing. Rats were fed diets containing TSK or magnesium oxide (MgO) to satisfy 25%, 50%, 75%, or 100% of their Mg requirements. We determined the relative Mg bioavailability of TSK compared to MgO and examined factors affecting Mg bioavailability in TSK. RESULTS: The relative bioavailability of Mg in TSK compared with MgO was calculated as 92.3%, 111.4%, and 87.2% from apparent absorption, urinary excretion, and femoral concentration of Mg, respectively. The ultrafiltrable Mg concentration was lower in the cecal content of rats given TSK than those given MgO. However, the mRNA expression of TRPM6, an Mg channel responsible for Mg absorption, was higher in the cecum of rats given TSK than those given MgO. CONCLUSION: Enhancement of TRPM6 expression in the large intestine negates the low bioaccessibility of Mg in TSK, and thus TSK shows Mg bioavailability comparable with MgO. © 2020 Society of Chemical Industry [ABSTRACT FROM AUTHOR]

Uncoupling protein 1 (UCP1) is responsible for non‐shivering thermogenesis, with restricted expression in brown/beige adipocytes in humans and rodents. We have previously shown an unexpected expression of UCP1 in bovine skeletal muscles. This study evaluated factors affecting Ucp1 gene expression in cultured bovine myogenic cells. Myosatellite cells, which were isolated from the bovine musculus longissimus cervicis, were induced to differentiate into myotubes in the presence of 2% horse serum. Previous studies using murine brown/beige adipocytes revealed that Ucp1 expression levels are directly increased by forskolin and all‐trans retinoic acid (RA). The transforming growth factor‐β (TGF‐β)/activin pathway negatively regulated Ucp1 expression, whereas activation of the bone morphogenetic protein (BMP) pathway indirectly increases Ucp1 expression through the stimulation of brown/beige adipogenesis. Neither forskolin nor RA significantly affected Ucp1 mRNA levels in bovine myogenic cells. A‐83‐01, an inhibitor of the TGF‐β/activin pathway, stimulated myogenesis in these cells. A‐83‐01 significantly increased the expression of some brown fat signature genes such as Pgc‐1α, Cox7a1, and Dio2, with a quantitative but not significant increase in the expression of Ucp1. Treatment with LDN‐193189, an inhibitor of the BMP pathway, did not affect the differentiation of bovine myosatellite cells. Rather, LDN‐193189 increased Ucp1 mRNA levels without modulating the levels of other brown/beige adipocyte‐related genes. The current results indicate that the regulation of Ucp1 expression in bovine myogenic cells is distinct from that in murine brown/beige adipocytes, which has been more intensely characterized. Significance of the study: We previously reported unexpected expression of Ucp1 in bovine muscle tissues; Ucp1 expression has been known to be detected predominantly in brown/beige adipocytes. This study examined regulatory expression of bovine Ucp1 in myogenic cells. Consistent with the changes in expression levels of brown/beige adipocyte‐selective genes, Ucp1 expression tended to be increased by inhibition of endogenous TGF‐β activity. In contrast, inhibition of endogenous BMP significantly increased Ucp1 expression without affecting brown/beige adipocyte‐selective gene expression. The current results indicate that regulatory expression of Ucp1 in bovine myogenic cells is distinct from that in murine brown/beige adipocytes that is more intensely characterized. [ABSTRACT FROM AUTHOR]