The effects of phenolic glycosides from Betula platyphylla var. japonica on adipocyte differentiation and mature adipocyte metabolism

Betula platyphylla var. japonica (Betulaceae) has been used traditionally in Asian countries for the treatment of inflammatory diseases. A recent study has reported a phenolic compound, platyphylloside from B. platyphylla, that shows inhibition on adipocyte differentiation and induces lipolysis in 3T3-L1 cells. Based on this finding, we conducted phytochemical analysis of the EtOH extract of the bark of B. platyphylla var. japonica, which resulted in the isolation of phenolic glycosides (1–4). Treatment of the isolated compounds (1–4) during adipocyte differentiation of 3T3-L1 mouse adipocytes resulted in dose-dependent inhibition of adipogenesis. In mature adipocytes, arylbutanoid glycosides (2–4) induced lipolysis related genes HSL and ATGL, whereas catechin glycoside (1) had no effect. Additionally, arylbutanoid glycosides (2–4) also induced GLUT4 and adiponectin mRNA expression, indicating improvement in insulin signaling. This suggests that the isolates from B. platyphylla var. japonica exert benefial effects in regulation of adipocyte differentiation as well as adipocyte metabolism.     

Warming Induces Significant Reprogramming of Beige,but Not Brown,Adipocyte Cellular Identity

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A novel brown adipocyte-enriched long non-coding RNA that is required for brown adipocyte differentiation and sufficient to drive thermogenic gene program in white adipocytes

The thermogenic activities of brown and beige adipocytes can be exploited to reduce energy surplus and counteract obesity. Recent RNA sequencing studies have uncovered a number of long noncoding RNAs (lncRNAs) uniquely expressed in white and brown adipose tissues (WAT and BAT), but whether and how these lncRNAs function in adipogenesis remain largely unknown. Here, we report the identification of a novel brown adipocyte-enriched LncRNA (AK079912), and its nuclear localization, function and regulation. The expression of AK079912 increases during brown preadipocyte differentiation and in response to cold-stimulated browning of white adipocytes. Knockdown of AK079912 inhibits brown preadipocyte differentiation, manifested by reductions in lipid accumulation and down-regulation of adipogenic and BAT-specific genes. Conversely, ectopic expression of AK079912 in white preadipocytes up-regulates the expression of genes involved in thermogenesis. Mechanistically, inhibition of AK079912 reduces mitochondrial copy number and protein levels of mitochondria electron transport chain (ETC) complexes, whereas AK079912 overexpression increases the levels of ETC proteins. Lastly, reporter and pharmacological assays identify Pparγ as an upstream regulator of AK079912. These results provide new insights into the function of non-coding RNAs in brown adipogenesis and regulating browning of white adipocytes.     

Ultrastructural and immunocytochemical studies of neuromuscular junctions in oviduct of Locusta migratoria

The ultrastructure of nerve endings in the oviduct visceral muscles of Locusta migratoria was studied by electron microscopy and by immunogold labeling for two kinds of neuromodulators, the pentapeptide proctolin and FMRFamide-related peptides. Nerve endings contained electron-lucent round vesicles and two kinds of granules (round and avoid), and formed two types of synapses or release sites with the muscle. The morphologically distinct nerve endings were classified into three different categories based on the composition of synaptic vesicles and granules. Type-I nerve endings were dominated by electron-lucent round vesicles and contained only a few round electron-dense granules. Type-II nerve endings contained mostly electron-dense round granules and electron-lucent round vesicles. A few electron-dense ovoid granules were also present. Electron-dense ovoid granules dominated the type-III nerve endings, which usually contained less electron-lucent vesicles than either type-I or II nerve endings. Both proctolin and FMRFamide-like immunoreactivity was associated with electron-dense round granules. However, FMRFamide-like immunoreactivity was only found in the type-II nerve endings, while proctolin immunoreactivity was found within type-I nerve endings as well as in some type-II nerve endings. Immunological results therefore allow us to further divide type-II nerve endings into type-IIa (immunonegative for proctolin) and type-IIb (immunopositive for proctolin). Type-III nerve endings show no immunolabeling to either proctolin or FMRFamide.     

The biological activity of duck ‘big’ somatostatin on chicken adipose tissue

A peptide, eluted with cytochrome c, called ‘big’ somatostatin, is the only somatostatin-like immunoreactivity present in the peripheral plasma of the duck. The metabolic action of partially purified fractions of ‘big’ somatostatin was investigated on glucagon-stimulated lipolysis in chicken adipocytes. Significant inhibition of glycerol release (an index of lipolysis) induced by physiological concentrations of glucagon was observed with physiological concentrations of ‘big’ somatostatin; the percentage of inhibition was dose-dependent.     

3′-Hydroxy-ε,ε-caroten-3-one inhibits the differentiation of 3T3-L1 cells to adipocytes

An oxidative metabolite of lutein, 3′-hydroxy-ε,ε-caroten-3-one, inhibited the differentiation of 3T3-L1 cells to adipocytes and the subsequent triacylglycerol production, but lutein did not. The α,β-unsaturated carbonyl structure of 3′-hydroxy-ε,ε-caroten-3-one was considered to participate in the inhibitory effect, suggesting that this lutein metabolite has the potential to prevent metabolic syndrome.     

Effects of islet-activating protein on insulin- and isoprenaline-stimulated glucose transport in isolated rat adipocytes

The effects of islet-activating protein (IAP), a Bordetella pertussis toxin, on insulin- and isoprenaline-stimulated glucose transport were studied in isolated rat adipocytes. Basal as well as insulin-stimulated glucose transport were not affected when cells were pretreated with IAP. In contrast, IAP pretreatment abolished the stimulatory effect of isoprenaline. When IAP-pretreated cells were exposed to a combination of insulin and isoprenaline, the catecholamine significantly reduced the stimulatory effect of insulin. Since IAP is supposed to specifically block the inhibitory component Ni of adenylate cyclase, the results suggest that: (a) the effect of insulin is unrelated to the regulation of adenylate cyclase; (b) isoprenaline may exert both stimulatory and inhibitory effects depending on activation of Ni. The inhibitory regulation of adenylate cyclase may thus be a pivotal link in the regulation of glucose transport.     

Ontogeny and nutritional control of adipogenesis in zebrafish (Danio rerio)

The global obesity epidemic demands an improved understanding of the developmental and environmental factors regulating fat storage. Adipocytes serve as major sites of fat storage and as regulators of energy balance and inflammation. The optical transparency of developing zebrafish provides new opportunities to investigate mechanisms governing adipocyte biology, however zebrafish adipocytes remain uncharacterized. We have developed methods for visualizing zebrafish adipocytes in vivo by labeling neutral lipid droplets with Nile Red. Our results establish that neutral lipid droplets first accumulate in visceral adipocytes during larval stages and increase in number and distribution as zebrafish grow. We show that the cellular anatomy of zebrafish adipocytes is similar to mammalian white adipocytes and identify peroxisome-proliferator activated receptor γ and fatty acid binding protein 11a as markers of the zebrafish adipocyte lineage. By monitoring adipocyte development prior to neutral lipid deposition, we find that the first visceral preadipocytes appear in association with the pancreas shortly after initiation of exogenous nutrition. Zebrafish reared in the absence of food fail to form visceral preadipocytes, indicating that exogenous nutrition is required for adipocyte development. These results reveal homologies between zebrafish and mammalian adipocytes and establish the zebrafish as a new model for adipocyte research.