Regulatory effects of the AMPKα-SIRT1 molecular pathway on insulin resistance in PCOS mice: An in vitro and in vivo study

Xin, Tao; Chen, Lei; Cai, Lixin; Ge, Shengfang; Deng, Xuanying

doi:10.1016/j.bbrc.2017.09.154

Cited by 31 publications

(31 citation statements)

References 25 publications

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“…PCOS patients are often accompanied by IR; our preliminary study has found the protective effects of AMPKα molecule in PCOS mice with IR [6], from this we speculate that PGC1α plays an important role in the pathogenesis of IR in PCOS. Based on the above assumptions, we conducted an in vivo PCOS mouse experiment to investigate the association between insulin resistance-related AMPKα pathway and PGCα in PCOS mice and to find out more molecular mechanisms and potential therapeutic targets for the pathogenesis of PCOS.…”

Section: Introductionmentioning

confidence: 51%

“…Previous results have showed that compared with PCOS group, the insulin sensitivity of the mice in the PA group improved (HOMA-IR = 7.621 ± 1.66 vs 10.133 ± 1.654, P < 0.05) and the estrous cycle became regular after 7 days of AICAR treatment, however, PCOS group and PC group are still in a status of insulin resistance (HOMA-IR = 10.765 ± 2.036 vs 10.133 ± 1.654, P < 0.05) after 7 days of Compound C treatment. In addition, androgen levels did not recover Open Journal of Endocrine and Metabolic Diseases significantly [6].…”

Section: Blood Samples and Ovarian Tissue Acquisition Modeling Andmentioning

confidence: 88%

“…Mice in the PCOS model group lost their regular estrous cycles and the model was considered successfully established [6]. Four PCOS mice and two control groups were randomly selected for fasting serum testosterone (T), fasting insulin (FINS), fasting plasma glucose (FGLU) detection, HOMA-IR index calculation and the ovarian HE staining was use to further assess the efficiency of model creation, the results of blood testing showed that: after pretreatment with DHEA for 20 days, the PCOS group was in an apparently insulin resistant state (P = 0.036) and serum testosterone was significantly elevated (P = 0.014) [6]. The remaining mice in the PCOS model group were randomly divided into the PA (PCOS + AICAR) group (n = 10), the PC (PCOS + compound C) group (n = 10) and the PCOS group (n = 7).…”

Section: Pcos Mouse Model Establishment and Reagent Interventionmentioning

confidence: 99%

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Explore the Relationship between Insulin Resistance and PGC1&alpha; in PCOS Mice

Chen¹,

Xin²,

Ge³

et al. 2018

OJEMD

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Objective: To investigate the relationship between AMPKα, PGCα, insulin resistance and reproductive function in PCOS mice and to find out the molecular mechanisms and potential therapeutic molecular targets of pathogenesis of PCOS. Methods: The PCOS mouse model was established by DHEA administering with Balb/c mice. And after AMPK agonist AICAR and inhibitor Compound C intervention, Fasting blood glucose, fasting insulin and testosterone levels were observed. The HOMA index was calculated. The changes of PGCα expression in ovarian tissue were observed by western blot and immunohistochemistry to determine the relationship between insulin resistance and PGCα in PCOS mice. Results: Western blot and immunohistochemistry showed that PGC1α protein was expressed in the ovary of mice and the expression of PGC1α was negatively correlated with AMPKα in our study. Compared with the control group, the expression of PGC1α in the ovaries of the mice in PCOS group was significantly increased (P < 0.05), after intervention with AMPK agonist AICAR, the expression of PGC1α in PCOS + AICAR group was lower than that in PCOS group (P < 0.05). It is worth noting that the expression of PGC1α in PCOS mice exposed to AMPK inhibitor Compound C also decreased compared with PCOS group (P < 0.05). Conclusion: In ovarian tissue, the insulin resistance-related AMPKα pathway in PCOS mice may be negatively correlated with PGCα.

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Section: Introductionmentioning

confidence: 51%

Section: Blood Samples and Ovarian Tissue Acquisition Modeling Andmentioning

confidence: 88%

Section: Pcos Mouse Model Establishment and Reagent Interventionmentioning

confidence: 99%

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Explore the Relationship between Insulin Resistance and PGC1&alpha; in PCOS Mice

Chen¹,

Xin²,

Ge³

et al. 2018

OJEMD

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“…The endometrium tissue collection and the hematoxylin-eosin (H&E) staining was done as previously described [7]. Endometrium tissue were placed in xylene and depara nized.…”

Section: Hematoxylin-eosin (Hande) Stainingmentioning

confidence: 99%

“…And SIRT1 agonist such as exenatide (EX) appeared to be superior to MET in restoring menstrual cycles and regulating metabolic disorders [6]. In our previous study [7,8], insulin resistance in PCOS rats was associated with the AMPKα-SIRT1 pathway. Furthermore, in our newly study showed that both EX and MET could improve the reproductive and endocrine functions of PCOS mice via the AMPKα-SIRT1 pathway, which may be the molecular mechanism for IR in PCOS and could possibly serve as a therapeutic target [9].…”

Section: Introductionmentioning

confidence: 99%

Exenatide Improves Endometrial Glands in PCOS Rats through AMPKα-SIRT1

Cai

et al. 2020

Preprint

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Exenatide can contribute to the therapeutic effect for PCOS patients in restoring menstrual cycles. To exploring endometrial tissue change in PCOS rats and the effects of exenatide on endometrial tissue, we carried out in vivo study of PCOS rat models. Method: PCOS rat models were obtained after DHEA treatment, and the corresponding parameters were measured to confirm the establishment of PCOS models. Hematoxylin-eosin (H&E) staining was performed to observe endometrium morphological change, and western blot and RT-PCR were performed to identify the alteration AMP-activated protein kinase (AMPKα) and SIRT1 proteins and the relative expression of SIRT1 mRNA in endometrial cellular after the intervention of exenatide (EX). Results: The endometrium of PCOS rats appeared to not only the gland number increased but also the gland size enlarged. When the PCOS rats underwent EX treatment, the gland number decreased and the gland size narrowed, the expression of AMPKα and SIRT1 protein increased, and the expression of SIRT1 mRNA level augmented. Conclusion: EX could decrease gland number and narrow gland size in PCOS rat endometrium which may be partly via AMPKα-SIRT1 pathway.

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Naringenin improves ovarian health by reducing the serum androgen and eliminating follicular cysts in letrozole‐induced polycystic ovary syndrome in the Sprague Dawley rats

Rashid,

Tripathi,

Singh

et al. 2023

Phytotherapy Research

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Polycystic ovary syndrome (PCOS) is most common in women of reproductive age, giving rise to androgen excess and anovulation, leading to infertility and non‐reproductive complications. We explored the ameliorating effect of naringenin in PCOS using the Sprague Dawley (SD) rat model and human granulosa cells. Letrozole‐induced PCOS rats were given either naringenin (50 mg/kg/day) alone or in combination with metformin (300 mg/kg/day), followed by the estrous cycle, hormonal analysis, and glucose sensitivity test. To evaluate the effect of naringenin on granulosa cell (hGC) steroidogenesis, we treated cells with naringenin (2.5 μM) alone or in combination with metformin (1 mM) in the presence of forskolin (10 μM). To determine the steroidogenesis of CYP‐17A1, ‐19A1, and 3βHSD2, the protein expression levels were examined. Treatment with naringenin in the PCOS animal groups increased ovulation potential and decreased cystic follicles and levels of androgens. The expression levels of CYP‐17A1, ‐19A1, and 3βHSD2, were seen restored in the ovary of PCOS SD rats' model and in the human ovarian cells in response to the naringenin. We found an increased expression level of phosphorylated‐AKT in the ovary and hGCs by naringenin. Naringenin improves ovulation and suppress androgens and cystic follicles, involving AKT activation.

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Regulatory effects of the AMPKα-SIRT1 molecular pathway on insulin resistance in PCOS mice: An in vitro and in vivo study

Cited by 31 publications

References 25 publications

Explore the Relationship between Insulin Resistance and PGC1&alpha; in PCOS Mice

Explore the Relationship between Insulin Resistance and PGC1&alpha; in PCOS Mice

Exenatide Improves Endometrial Glands in PCOS Rats through AMPKα-SIRT1

Naringenin improves ovarian health by reducing the serum androgen and eliminating follicular cysts in letrozole‐induced polycystic ovary syndrome in the Sprague Dawley rats

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Regulatory effects of the AMPKα-SIRT1 molecular pathway on insulin resistance in PCOS mice: An in vitro and in vivo study

Cited by 31 publications

References 25 publications

Explore the Relationship between Insulin Resistance and PGC1&amp;alpha; in PCOS Mice

Explore the Relationship between Insulin Resistance and PGC1&amp;alpha; in PCOS Mice

Exenatide Improves Endometrial Glands in PCOS Rats through AMPKα-SIRT1

Naringenin improves ovarian health by reducing the serum androgen and eliminating follicular cysts in letrozole‐induced polycystic ovary syndrome in the Sprague Dawley rats

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Product

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Explore the Relationship between Insulin Resistance and PGC1α in PCOS Mice

Explore the Relationship between Insulin Resistance and PGC1α in PCOS Mice