Cho-Rong Bae

Quercetin‐rich onion peel extract suppresses adipogenesis by down‐regulating adipogenic transcription factors and gene expression in 3T3‐L1 adipocytes

BACKGROUND Onion peel contains a high amount of quercetin, which has been reported to have anti-cholesterol, antithrombotic and insulin-sensitizing properties. This study aimed to elucidate the anti-adipogenic effects of quercetin-rich onion peel extract (OPE) and to compare it with commercially available quercetin using 3T3-L1 preadipocytes. RESULTS Without affecting cell viability, both OPE and quercetin averted adipogenesis, as characterized by dose-dependent decreases in intracellular triglyceride content and glycerol 3-phosphate dehydrogenase activity, but the effect was more pronounced with OPE than with quercetin. The mRNA expression levels of key adipogenic genes such as PPARγ, C/EBPα, FABP4, aP2 and LPL were decreased in a dose-dependent manner by both OPE and quercetin. CONCLUSION The results indicate that OPE treatment significantly prevents intracellular lipid accumulation via hyperactivation of genes regulating lipolysis as compared with quercetin alone.

Possible involvement of melanocortin-4-receptor and AMP-activated protein kinase in the interaction of glucagon-like peptide-1 and leptin on feeding in rats

Glucagon-like peptide-1 (GLP-1) and leptin are anorectic hormones produced in the small intestine and white adipose tissue, respectively. Investigating how these hormones act together as an integrated anorectic signal is important to elucidate a mechanism to maintain energy balance. In the present study, coadministration of subthreshold GLP-1 and leptin dramatically reduced feeding in rats. Although coadministration of GLP-1 with leptin did not enhance leptin signal transduction in the hypothalamus, it significantly decreased phosphorylation of AMP-activated protein kinase (AMPK). In addition, coadministration of GLP-1 with leptin significantly increased proopiomelanocortin (POMC) mRNA levels. Considering that α-melanocortin stimulating hormone (α-MSH) is derived from POMC and functions through the melanocortin-4-receptor (MC4-R) as a key molecule involved in feeding reduction, the interaction of GLP-1 and leptin on feeding reduction may be mediated through the α-MSH/MC4-R system. As expected, the interaction of GLP-1 and leptin was abolished by intracerebroventricular preadministration of the MC4-R antagonists agouti-related peptide and SHU9119. Taken together, GLP-1 and leptin cooperatively reduce feeding at least in part via inhibition of AMPK following binding of α-MSH to MC4-R.

Possible involvement of food texture in insulin resistance and energy metabolism in male rats

Food texture is known to affect energy metabolism. Although feeding with soft pellets (SP) or via a tube is known to cause increases in body weight, it is unclear how different food textures influence energy metabolism. In this study, we investigated the effects of two different food textures on energy balance and glucose and lipid metabolism in male Wistar rats. The rats were fed SP or control pellets (CP) on a 3-h restricted feeding schedule for 14 weeks and their energy intake, body weight, and energy expenditure were examined. The levels of gastrointestinal hormones, glucose and insulin, were investigated at pre-, mid, and post-feeding. Glucose tolerance and insulin tolerance tests were conducted, and the expressions of molecules involved in the insulin signaling system or lipogenesis in the liver were examined. Histological investigation of pancreatic islets was carried out using anti-insulin and anti-Ki-67 antibodies. Furthermore, the expression in the liver and circulating blood of microRNA-33 (miR-33), which regulates insulin receptor substance 2, was examined. There were no significant differences in energy intake, body weight, or gastrointestinal hormone levels between the SP and CP rats; however, the SP rats showed glucose intolerance and insulin resistance with disruption of insulin signaling. Increases in lipogenic factors and miR-33 expression were also found in the SP rats. The numbers of insulin-positive areas and Ki-67-positive cells of SP rats were significantly increased. This study shows that a soft food texture causes diabetes without obesity, so differences in food texture may be an important factor in type 2 diabetes.

Guanylin-Guanylyl cyclase-C signaling in macrophages regulates mesenteric fat inflammation induced by high-fat diet

Guanylin (Gn), a bioactive peptide, and its receptor, guanylyl cyclase-C (GC-C), are primarily present in the intestine and maintain homeostasis in body fluids. Recently, rats whose macrophages overexpress Gn and GC-C were found to be resistant to diet-induced obesity. Considering that obesity is strongly related to a chronic inflammatory state in white adipose tissues, it is possible that Gn-GC-C macrophages contribute to the regulation of inflammation. In the present study, we investigated the inflammatory state of mesenteric fat in rats transgenic for both Gn and GC-C (double-transgenic [dTg] rats) by evaluating the levels of cyclic guanosine monophosphate (cGMP), a second messenger of Gn-GC-C, cGMP-dependent protein kinase (PKG), and phosphorylated vasodilator-stimulated phosphoprotein (VASP), a target protein of PKG. The levels of cGMP in dTg rats was higher than in WT rats fed the same diet. Although there were no significant differences in levels of PKG and phosphorylated VASP between WT and dTg rats fed a standard diet (STD), these levels in dTg rats fed a high fat diet (HFD) were markedly increased compared with levels in HFD WT rats. Furthermore, mRNA levels of proinflammatory factors in mesenteric fat were lower in HFD dTg rats than in HFD WT rats and were similar to levels in STD WT and dTg rats. These results indicate that the Gn-GC-C system in macrophages regulates the cGMP-PKG-VASP pathway and controls obesity through the downregulation of proinflammatory factors.

Anti-obesity effects of traditional and standardized meju in high-fat diet-induced obese C57BL/6J mice

The aim of the study was to evaluate the anti-obesity effects of two types of meju in diet induced obese C57BL/6J mice. Animals were randomly divided into 4 dietary group (n = 10); normal diet, high fat diet with 30% soybean, high fat diet with 30% traditional meju, high fat diet with 30% standardized meju. After 16 weeks, after animals were sacrificed. It was observed that the high fat diet with 30% traditional meju and high fat diet with 30% standardized meju significantly reduced body weight gain, epididymal fat weight, serum triglyceride along with serum insulin and leptin levels compared to the high fat diet with 30% soybean. And also, the expression levels of hepatic lipid anabolic genes were significantly decreased in the high fat diet with 30% traditional meju and high fat diet with 30% standardized meju compared to the high fat diet with 30% soybean. In conclusion, the assessment of all the obesity markers strongly advocate the anti-obesity effect of traditional as well as standardized meju in diet induce obesity conditions.

The Short-Term Effects of Soft Pellets on Lipogenesis and Insulin Sensitivity in Rats

The purpose of the present study was to investigate the short-term effects of a 12-day, soft pellet (SP) diet with a 3-h restricted feeding schedule on caloric intake, body weight, lipid metabolism, and insulin sensitivity. Glucose and insulin levels were measured pre-, mid-, and post-feeding. The SP rats exhibited postprandial hyperglycemia compared to rats fed control pellets (CP). The insulin response of SP rats during a meal was significantly higher than that of CP rats. There were no significant differences in the hepatic triacylglycerol contents and lipogenesis gene mRNA levels of SP and CP rats. However, the hepatocytes of SP rats were slightly hypertrophic. In addition, histological analysis revealed that the pancreases of SP rats had more islet areas than those of CP rats. This study demonstrated that feeding an SP-only diet for 12 days induces glucose intolerance, suggesting that the consumption of absorbable food, like a soft diet, may trigger glucose metabolism insufficiency and lead to life-threatening diseases.