Combination of metformin and exercise alleviates osteoarthritis in ovariectomized mice fed a high-fat diet

Bone ◽  
2022 ◽  
pp. 116323
Author(s):  
Hetong Li ◽  
Yu Gou ◽  
Faming Tian ◽  
Ya Zhang ◽  
Qiangqiang Lian ◽  
...  
Keyword(s):  
High Fat Diet ◽  
High Fat ◽  
Ovariectomized Mice

scholarly journals Tea Seed Oil Prevents Obesity, Reduces Physical Fatigue, and Improves Exercise Performance in High-Fat-Diet-Induced Obese Ovariectomized Mice

Molecules ◽  
2019 ◽  
Vol 24 (5) ◽  
pp. 980 ◽  
Author(s):  
Yu-Tang Tung ◽  
Yi-Ju Hsu ◽  
Yi-Wen Chien ◽  
Chi-Chang Huang ◽  
Wen-Ching Huang ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Exercise Performance ◽  
High Fat Diet ◽  
Seed Oil ◽  
Physical Fatigue ◽  
High Fat ◽  
Tea Seed Oil ◽  
Ovariectomized Mice ◽  
Total Fat

Menopause is associated with changes in body composition (a decline in lean body mass and an increase in total fat mass), leading to an increased risk of metabolic syndrome, nonalcoholic fatty liver disease, and heart disease. A healthy diet to control body weight is an effective strategy for preventing and treating menopause-related metabolic syndromes. In the present study, we investigated the effect of long-term feeding of edible oils (soybean oil (SO), tea seed oil (TO), and lard oil (LO)) on female ovariectomized (OVX) mice. SO, TO, and LO comprise mainly polyunsaturated fatty acids (PUFA), monounsaturated fatty acids (MUFA), and saturated fatty acids (SFA), respectively. However, there have been quite limited studies to investigate the effects of different fatty acids (PUFA, MUFA, and SFA) on physiological adaption and metabolic homeostasis in a menopausal population. In this study, 7-week-old female Institute of Cancer Research (ICR) mice underwent either bilateral laparotomy (sham group, n = 8) or bilateral oophorectomy (OVX groups, n = 24). The OVX mice given a high-fat diet (HFD) were randomly divided into three groups: OVX+SO, OVX+TO, and OVX+LO. An HFD rich in SO, TO, or LO was given to the OVX mice for 12 weeks. Our findings revealed that the body weight and relative tissues of UFP (uterus fatty peripheral) and total fat (TF) were significantly decreased in the OVX+TO group compared with those in the OVX+SO and OVX+LO groups. However, no significant difference in body weight or in the relative tissues of UFP and TF was noted among the OVX+SO and OVX+LO groups. Furthermore, mice given an HFD rich in TO exhibited significantly decreased accumulation of liver lipid droplets and adipocyte sizes of UFP and brown adipose tissue (BAT) compared with those given an HFD rich in SO or LO. Moreover, replacing SO or LO with TO significantly increased oral glucose tolerance. Additionally, TO improved endurance performance and exhibited antifatigue activity by lowering ammonia, blood urea nitrogen, and creatine kinase levels. Thus, tea seed oil (TO) rich in MUFA could prevent obesity, reduce physical fatigue, and improve exercise performance compared with either SO (PUFA)- or LO(SFA)-rich diets in this HFD-induced obese OVX mice model.

scholarly journals Luteolin Improves Insulin Resistance in Postmenopausal Obese Mice by Altering Macrophage Polarization (FS12-01-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Yunjung Baek ◽  
Mi Nam Lee ◽  
Dayong Wu ◽  
Munkyong Pae
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Ovarian Function ◽  
Body Weight Gain ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Ovariectomized Mice

Abstract Objectives Previously, we showed that loss of ovarian function in mice fed high-fat diet exacerbated insulin resistance and adipose tissue inflammation. In the current study, we tested whether consumption of luteolin, an anti-inflammatory flavonoid, could mitigate adipose tissue inflammation and insulin resistance in obese ovariectomized mice. Methods Nine-week-old ovariectomized C57BL/6 mice were fed a low-fat diet (LFD), high-fat diet (HFD), or HFD supplemented with 0.005% luteolin (HFD + L) for 16 weeks. The anti-inflammatory drug salicylate was used as a positive control. Fasting blood glucose, insulin, and insulin resistance index HOMA-IR were measured every 4 weeks. Adipose tissue and spleen were characterized for tissue inflammation by real-time PCR and immune cell populations by flow cytometry after 16 weeks of feeding. Results HFD resulted in more body weight gain than LFD in ovariectomized mice and supplementing HFD with 0.005% luteolin did not affect the body weight gain. In addition, HFD elicited a significant elevation in fat mass, which were comparable between HFD and HFD + L groups. However, luteolin supplementation resulted in a significant decrease in CD11c+ macrophages in gonadal adipose tissue, as well as a trend of decrease in macrophage infiltration. Luteolin supplementation also significantly decreased mRNA expression of inflammatory and M1 markers MCP-1, CD11c, TNF-a, and IL-6, while maintaining expression of M2 marker MGL1. We further found that luteolin treatment protected mice from insulin resistance induced by HFD consumption; this improved insulin resistance was correlated with reductions in CD11c+ adipose tissue macrophages. Conclusions Our findings indicate that dietary luteolin supplementation attenuates adipose tissue inflammation and insulin resistance found in mice with loss of ovarian function coupled with a HFD intake, and this effect may be partly mediated through suppressing M1-like polarization of macrophages in adipose tissue. These results have clinical implication in implementing dietary intervention for prevention of metabolic syndrome associated with postmenopause and obesity. Funding Sources Supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (NRF-2018R1A1A1A05078886).

scholarly journals Estradiol Prevents Fat Accumulation and Overcomes Leptin Resistance in Female High-Fat Diet Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (11) ◽  
pp. 4447-4460 ◽  
Author(s):  
Sara A. Litwak ◽  
Jenny L. Wilson ◽  
Weiyi Chen ◽  
Cecilia Garcia-Rudaz ◽  
Mohammad Khaksari ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Fat Content ◽  
Leptin Resistance ◽  
Whole Body ◽  
High Fat ◽  
Fat Accumulation ◽  
The Metabolic Syndrome ◽  
Ovariectomized Mice

AbstractIn premenopausal and menopausal women in particular, suboptimal estrogens have been linked to the development of the metabolic syndrome as major contributors to fat accumulation. At the same time, estrogens have been described to have a role in regulating body metabolic status. We evaluated how endogenous or administered estrogens impact on the changes associated with high-fat diet (HFD) consumption in 2 different paradigms; ovarian-intact and in ovariectomized mice. When estradiol (E2) was cyclically administered to ovarian-intact HFD-fed mice for 12 weeks, animals gained significantly less weight than ovarian-intact vehicle controls (P < .01). This difference was mainly due to a reduced caloric intake but not to an increase in energy expenditure or locomotor activity. This E2 treatment regime to mice exposed to HFD was overall able to avoid the increase of visceral fat content to levels of those found in mice fed a regular chow diet. In the ovariectomized model, the main body weight and fat content reducing action of E2 was not only through decreasing food intake but also by increasing the whole-body energy expenditure, locomotor activity, and by inducing fat oxidation. Importantly, these animals became responsive to the anorexigenic effects of leptin in contrast to the vehicle-treated and the pair-fed control groups (P < .01). Further, in vitro hypothalamic secretion experiments revealed that treatment of obese mice with E2 is able to modulate the secretion of appetite-regulating neuropeptides; namely, E2 increased the secretion of the anorectic neuropeptide α-melanocyte-stimulating hormone and decreased the secretion of the orexigenic neuropetides neuropeptide Y and Agouti-related peptide. In conclusion, differences in response to E2 treatment of HFD-fed animals depend on their endogenous estrogenic status. Overall, E2 administration overcomes arcuate leptin resistance and partially prevents fat accumulation on these mice.

scholarly journals GIP receptor antagonist treatment causes weight loss in ovariectomized high fat diet-fed mice

2021 ◽  
Author(s):  
Geke Aline Boer ◽  
Jenna Hunt ◽  
Maria Gabe ◽  
Johanne Windeløv ◽  
Alexander Sparre-Ulricht ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Pharmacokinetic Profile ◽  
High Fat ◽  
Ovariectomized Mice ◽  
Gip Receptor

Background and purpose The incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), secreted by the enteroendocrine K-cells in the proximal intestine, may regulate lipid metabolism and adiposity but its exact role in these processes is unclear. Experimental approach We characterized in vitro and in vivo antagonistic properties of a novel GIP analogue, mGIPAnt-1. We further assessed the in vivo pharmacokinetic profile of this antagonist, as well as its ability to affect high-fat diet (HFD)-induced body weight gain in ovariectomized mice during an 8-week treatment period. Key results mGIPAnt-1 showed competitive antagonistic properties to the GIP receptor (GIPR) in vitro as it inhibited GIP-induced cAMP accumulation in COS-7 cells. Furthermore, mGIPAnt-1 was capable of inhibiting GIP-induced glucoregulatory and insulinotropic effects in vivo and has a favourable pharmacokinetic profile with a half-life of 7.2 hours in C57Bl6 female mice. Finally, sub-chronic treatment with mGIPAnt-1 in ovariectomized HFD mice resulted in a reduction of body weight and fat mass. Conclusion and Implications mGIPAnt-1 successfully inhibited acute GIP-induced effects in vitro and in vivo and sub-chronically induces resistance to HFD-induced weight gain in ovariectomized mice. Our results support the development of GIP antagonists for the therapy of obesity.

Vascular dysfunction and impaired insulin signaling in high-fat diet fed ovariectomized mice

2011 ◽  
Vol 82 (2) ◽  
pp. 171-176 ◽  
Author(s):  
Koji Tominaga ◽  
Atsushi Yamauchi ◽  
Takashi Egawa ◽  
Ryosuke Tanaka ◽  
Satoko Kawahara ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
High Fat Diet ◽  
Vascular Dysfunction ◽  
High Fat ◽  
Ovariectomized Mice ◽  
Impaired Insulin

Raloxifene Ameliorates Liver Fibrosis of Nonalcoholic Steatohepatitis Induced by Choline-Deficient High-Fat Diet in Ovariectomized Mice

2015 ◽  
Vol 60 (9) ◽  
pp. 2730-2739 ◽  
Author(s):  
Fangqiong Luo ◽  
Masatoshi Ishigami ◽  
Koichi Achiwa ◽  
Yoji Ishizu ◽  
Teiji Kuzuya ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
High Fat ◽  
Ovariectomized Mice

scholarly journals The PCSK9 Involves in the Dyslipidemia of Ovariectomized Mice and Its Mechanism

2021 ◽  
Author(s):  
Dan Zhao ◽  
Xue-qin Zhang ◽  
Wen-jing Guo ◽  
Zhi-hui Cui ◽  
Yi-cheng Wang ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Cholesterol Metabolism ◽  
Critical Role ◽  
Normal Diet ◽  
High Fat ◽  
Lipid Metabolism Disorder ◽  
Pcsk9 Inhibitor ◽  
Metabolism Disorder ◽  
Ovariectomized Mice

Abstract Ovarian failure in postmenopausal female leads E2 to dramatic decrease which is an important reason of menopausal dyslipidemia. PCSK9 as a secretory lipid metabolic regulator plays a critical role in the cholesterol metabolism by negatively regulating LDLR in hepatocytes. Clinical data showed PCSK9 was elevated and positively correlated with LDL-C in the blood of postmenopausal women. However, the relationship between E2 and PCSK9 and the role of PCSK9 in postmenopausal dyslipidemia are still unclear. In this research, 10-week-old ovariectomized mice were fed for 4 weeks with normal diet or high-fat diet, then tested the lipid metabolism profiles and PCSK9 in the blood and the expression of LDLR and PCSK9 in the liver. On this basis, PCSK9-/- ovariectomized mice were used to further verify the effect of PCSK9 in dyslipidemia of ovariectomized mice. Finally, the ovariectomized mice with high-fat diet were subcutaneous injected respectively with E2 or PCSK9 inhibitor alone or both together for 2 weeks and were tested as previous experiment. The results showed PCSK9, TC and LDL-c all increased in the blood of in WT ovariectomized mice and their PCSK9 is positively correlated with LDL-c, while there were on obvious lipid metabolism disorder in the PCSK9−/− ovariectomized mice. PCSK9 inhibitor increased the LDLR on the liver and ameliorated the dyslipidemia in WT ovariectomized mice. It suggests that PCSK9 plays an important role in the dyslipidemia of ovariectomized mice, which provides a new strategy for clinical diagnosis and treatment of the dyslipidemia in post-menopause.

scholarly journals Estradiol regulates daily rhythms underlying diet-induced obesity in female mice

2019 ◽  
Vol 317 (6) ◽  
pp. E1172-E1181 ◽  
Author(s):  
Oluwabukola Omotola ◽  
Sandra Legan ◽  
Emily Slade ◽  
Ayooluwatomiwa Adekunle ◽  
Julie S. Pendergast
Keyword(s):  
Circadian Rhythms ◽  
Eating Behavior ◽  
High Fat Diet ◽  
Circadian System ◽  
High Fat ◽  
Daily Rhythms ◽  
Diet Induced Obesity ◽  
Ovariectomized Mice ◽  
Circulating Levels

The circadian system is a critical regulator of metabolism and obesity in males, but its role in regulating obesity in females is poorly understood. Because there are sex differences in the development of obesity and susceptibility to obesity-related disorders, we sought to determine the role of estrogens in regulating the circadian mechanisms underlying diet-induced obesity. When fed high-fat diet, C57BL/6J male mice gain weight, whereas females are resistant to diet-induced obesity. Here, we demonstrate that estradiol regulates circadian rhythms in females to confer resistance to diet-induced obesity. We found that ovariectomized females with undetectable circulating estrogens became obese and had disrupted daily rhythms of eating behavior and locomotor activity when fed a high-fat diet. The phase of the liver molecular circadian rhythm was also altered by high-fat diet feeding in ovariectomized mice. Estradiol replacement in ovariectomized females a fed high-fat diet rescued these behavioral and tissue rhythms. Additionally, restoring the daily rhythm of eating behavior in ovariectomized females with time-restricted feeding inhibited diet-induced obesity and insulin resistance. Together, these data suggest that the circadian system is a target for treating obesity and its comorbidities in women after menopause, when circulating levels of estrogens are too low to protect their circadian rhythms.

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