Obesity and diabetes gene loci in genetically obese mice

2000 ◽  
Vol 151 (1) ◽  
pp. 86
Author(s):  
AlanD. Attie ◽  
Jonathan Stoehr ◽  
Samuel Nadler ◽  
Mary Rabaglia ◽  
Brian Yandell ◽  
...  
Keyword(s):  
Obese Mice ◽  
Obesity And Diabetes ◽  
Diabetes Gene

Obesity and Diabetes Gene Discovery Approaches

2003 ◽  
Vol 9 (17) ◽  
pp. 1357-1372 ◽  
Author(s):  
K. Walder ◽  
D. Segal ◽  
J. Jowett ◽  
J. Blangero ◽  
G. Collier
Keyword(s):  
Gene Discovery ◽  
Obesity And Diabetes ◽  
Diabetes Gene

Obesity and Diabetes Gene Discovery Approaches

2005 ◽  
Vol 2 (1) ◽  
pp. 161-182
Author(s):  
Ken Walder ◽  
David Segal ◽  
Jeremy Jowett ◽  
John Blangero ◽  
Greg R. Collier
Keyword(s):  
Gene Discovery ◽  
Obesity And Diabetes ◽  
Diabetes Gene

scholarly journals ­Myostain is Involved in GINSENOSIDE-Rb1-mediated anti-obesity

2021 ◽  
Author(s):  
Hong-Shi Li ◽  
Jiang-Ying Kuang ◽  
Gui-Jun Liu ◽  
Wei-Jie Wu ◽  
Xian-Lun Yin ◽  
...  
Keyword(s):  
Active Component ◽  
C2c12 Cells ◽  
Ginsenoside Rb1 ◽  
Obese Mice ◽  
Reduced Body ◽  
Obesity And Diabetes ◽  
The World ◽  
Treatment Of Obesity ◽  
Myoblast Cells

Abstract Obesity, as one of the major public health problems in the world, has attracted more and more attention. Rb1 is the most abundant active component of Panax ginseng and it has been reported to have benefit effects on obesity and diabetes. But the mechanisms of Rb1 in regulation of obesity are not very clear. In this study, by use of obese mice, we found that Rb1 not only reduced body weight but also decreased myostain (MSTN) expression,which plays a vital part in the regulation of obesity. In vitro, we found that Rb1 treatment also decreased MSTN expression in differentiated C2C12 cells (Myoblast cells) and 3T3-L1 cells (adipocytes). Fndc5, as the downstream of MSTN, was increased after Rb1 treatment. ConclusionsOur results showed that Rb1 may ameliorate obesity in part through MSTN/Fndc5 signaling pathway. Our study provides important experimental evidences for the treatment of obesity by Rb1.

scholarly journals Obesity and Diabetes Gene Discovery Approaches

2012 ◽  
pp. 161-182
Author(s):  
Ken Walder ◽  
David Segal ◽  
Jeremy Jowett ◽  
John Blangero ◽  
Greg R. Collier
Keyword(s):  
Gene Discovery ◽  
Obesity And Diabetes ◽  
Diabetes Gene

scholarly journals Gut microbiota-based vaccination engages innate immunity to improve blood glucose control in obese mice

2021 ◽  
Author(s):  
Brittany M Duggan ◽  
Akhilesh K Tamrakar ◽  
Nicole G Barra ◽  
Fernando F Anhe ◽  
Gabriella Paniccia ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Blood Glucose ◽  
Gut Microbiota ◽  
Glucose Control ◽  
Subcutaneous Injection ◽  
Blood Glucose Control ◽  
Dependent Manner ◽  
Obese Mice ◽  
Bacterial Extract ◽  
Obesity And Diabetes

Obesity and diabetes increase circulating levels of microbial components derived from the gut microbiota. Individual bacterial factors (i.e., postbiotics) can have opposing effects on metabolic inflammation and blood glucose control. We tested the net effect of gut bacterial extracts on blood glucose using a microbiota-based vaccination strategy in mice. Male and female mice had improved insulin sensitivity and blood glucose control five weeks after a single subcutaneous injection of a specific dose of a bacterial extract obtained from the luminal contents of the proximal gut. Injection of mice with proximal gut extracts from germ-free mice revealed that bacteria were required for a microbiota-based vaccination to improve blood glucose control. Vaccination of Nod1-/-, Nod2-/-, and Ripk2-/- mice showed that each of these innate immune proteins was required for bacterial extract injection to improve blood glucose control. A microbiota-based vaccination promoted a proximal gut immunoglobulin-G (IgG) response directed against bacterial extract antigens, where subcutaneous injection of mice with the luminal contents of the ileum elicited a bacterial extract-specific IgG response that is compartmentalized to the ileum of vaccinated mice. A microbiota-based vaccination was associated with an altered the microbiota composition in the ileum and colon of mice. Lean mice required a single injection of proximal gut bacterial extracts, but high fat diet (HFD)-fed, obese mice required prime-boost bacterial extract injections for improvements in blood glucose control. These data show that, upon subversion of the gut barrier, vaccination with proximal gut bacterial extracts engages innate immunity to promote long-lasting improvements in blood glucose control in a dose-dependent manner.

scholarly journals Chrysanthemum Leaf Ethanol Extract Prevents Obesity and Metabolic Disease in Diet-Induced Obese Mice via Lipid Mobilization in White Adipose Tissue

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1347 ◽  
Author(s):  
Ri Ryu ◽  
Eun-Young Kwon ◽  
Ji-Young Choi ◽  
Jong Cheol Shon ◽  
Kwang-Hyeon Liu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
White Adipose Tissue ◽  
Ethanol Extract ◽  
The Body ◽  
Obese Mice ◽  
Peripheral Tissues ◽  
Lipid Mobilization ◽  
Obesity And Diabetes ◽  
Brown Adipose

This study aimed to elucidate the molecular mechanism of Chrysanthemum morifolium Ramat. against obesity and diabetes, by comparing the transcriptional changes in epididymal white adipose tissue (eWAT) with those of the bioactive compound in C. morifolium, luteolin (LU). Male C57BL/6J mice were fed a normal diet, high-fat diet (HFD), and HFD supplemented with 1.5% w/w chrysanthemum leaf ethanol extract (CLE) for 16 weeks. Supplementation with CLE and LU significantly decreased the body weight gain and eWAT weight by stimulating mRNA expressions for thermogenesis and energy expenditure in eWAT via lipid mobilization, which may be linked to the attenuation of dyslipidemia. Furthermore, CLE and LU increased uncoupling protein-1 protein expression in brown adipose tissue, leading to energy expenditure. Of note, CLE and LU supplements enhanced the balance between lipid storage and mobilization in white adipose tissue (WAT), in turn, inhibiting adipocyte inflammation and lipotoxicity of peripheral tissues. Moreover, CLE and LU attenuated hepatic steatosis by suppressing hepatic lipogenesis, thereby ameliorating insulin resistance and dyslipidemia. Our data suggest that CLE helps inhibit obesity and its comorbidities via the complex interplay between liver and WAT in diet-induced obese mice.

scholarly journals Lipocalin-2 counteracts metabolic dysregulation in obesity and diabetes

2020 ◽  
Vol 217 (10) ◽  
Author(s):  
Ioanna Mosialou ◽  
Steven Shikhel ◽  
Na Luo ◽  
Peristera Ioanna Petropoulou ◽  
Konstantinos Panitsas ◽  
...  
Keyword(s):  
Food Intake ◽  
Glucose Metabolism ◽  
Cell Function ◽  
Endocrine Function ◽  
Protective Mechanism ◽  
Lipocalin 2 ◽  
Obese Mice ◽  
Β Cell ◽  
Obesity And Diabetes ◽  
Β Cell Function

Regulation of food intake is a recently identified endocrine function of bone that is mediated by Lipocalin-2 (LCN2). Osteoblast-secreted LCN2 suppresses appetite and decreases fat mass while improving glucose metabolism. We now show that serum LCN2 levels correlate with insulin levels and β-cell function, indices of healthy glucose metabolism, in obese mice and obese, prediabetic women. However, LCN2 serum levels also correlate with body mass index and insulin resistance in the same individuals and are increased in obese mice. To dissect this apparent discrepancy, we modulated LCN2 levels in mice. Silencing Lcn2 expression worsens metabolic dysfunction in genetic and diet-induced obese mice. Conversely, increasing circulating LCN2 levels improves metabolic parameters and promotes β-cell function in mouse models of β-cell failure acting as a growth factor necessary for β-cell adaptation to higher metabolic load. These results indicate that LCN2 up-regulation is a protective mechanism to counteract obesity-induced glucose intolerance by decreasing food intake and promoting adaptive β-cell proliferation.

scholarly journals Effects of vitamin D deficiency on the improvement of metabolic disorders in obese mice after vertical sleeve gastrectomy

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jie Zhang ◽  
Min Feng ◽  
Lisha Pan ◽  
Feng Wang ◽  
Pengfei Wu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vitamin D ◽  
Weight Loss ◽  
Sleeve Gastrectomy ◽  
Vitamin D Deficiency ◽  
Hepatic Steatosis ◽  
Metabolic Disorders ◽  
Obese Mice ◽  
Vertical Sleeve Gastrectomy ◽  
Obesity And Diabetes

AbstractVertical sleeve gastrectomy (VSG) is one of the most commonly performed clinical bariatric surgeries for the remission of obesity and diabetes. Its effects include weight loss, improved insulin resistance, and the improvement of hepatic steatosis. Epidemiologic studies demonstrated that vitamin D deficiency (VDD) is associated with many diseases, including obesity. To explore the role of vitamin D in metabolic disorders for patients with obesity after VSG. We established a murine model of diet-induced obesity + VDD, and we performed VSGs to investigate VDD's effects on the improvement of metabolic disorders present in post-VSG obese mice. We observed that in HFD mice, the concentration of VitD3 is four fold of HFD + VDD one. In the post-VSG obese mice, VDD attenuated the improvements of hepatic steatosis, insulin resistance, intestinal inflammation and permeability, the maintenance of weight loss, the reduction of fat loss, and the restoration of intestinal flora that were weakened. Our results suggest that in post-VSG obese mice, maintaining a normal level of vitamin D plays an important role in maintaining the improvement of metabolic disorders.

Increased GIP signaling induces adipose inflammation via a HIF-1α-dependent pathway and impairs insulin sensitivity in mice

2015 ◽  
Vol 308 (5) ◽  
pp. E414-E425 ◽  
Author(s):  
Shu Chen ◽  
Fumiaki Okahara ◽  
Noriko Osaki ◽  
Akira Shimotoyodome
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Adipose Tissue Inflammation ◽  
Obese Mice ◽  
Plasminogen Activator Inhibitor 1 ◽  
Tissue Inflammation ◽  
Obesity And Diabetes ◽  
Gut Hormone

Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone secreted in response to dietary fat and glucose. The blood GIP level is elevated in obesity and diabetes. GIP stimulates proinflammatory gene expression and impairs insulin sensitivity in cultured adipocytes. In obesity, hypoxia within adipose tissue can induce inflammation. The aims of this study were 1) to examine the proinflammatory effect of increased GIP signaling in adipose tissues in vivo and 2) to clarify the association between GIP and hypoxic signaling in adipose tissue inflammation. We administered GIP intraperitoneally to misty (lean) and db/db (obese) mice and examined adipose tissue inflammation and insulin sensitivity. We also examined the effects of GIP and hypoxia on expression of the GIP receptor (GIPR) gene and proinflammatory genes in 3T3-L1 adipocytes. GIP administration increased monocyte chemoattractant protein-1 (MCP-1) expression and macrophage infiltration into adipose tissue and increased blood glucose in db/db mice. GIPR and hypoxia-inducible factor-1α (HIF-1α) expressions were positively correlated in the adipose tissue in mice. GIPR expression increased dramatically in differentiated adipocytes. GIP treatment of adipocytes increased MCP-1 and interleukin-6 (IL-6) production. Adipocytes cultured either with RAW 264 macrophages or under hypoxia expressed more GIPR and HIF-1α, and GIP treatment increased gene expression of plasminogen activator inhibitor 1 and IL-6. HIF-1α gene silencing diminished both macrophage- and hypoxia-induced GIPR expression and GIP-induced IL-6 expression in adipocytes. Thus, increased GIP signaling plays a significant role in adipose tissue inflammation and thereby insulin resistance in obese mice, and HIF-1α may contribute to this process.

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