scholarly journals Sex Hormones and Their Receptors Regulate Liver Energy Homeostasis

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Minqian Shen ◽  
Haifei Shi
Keyword(s):  
Estrogen Receptors ◽  
Hepatic Steatosis ◽  
Sex Hormones ◽  
Energy Homeostasis ◽  
Hormone Receptors ◽  
Androgen Receptors ◽  
Glycogen Synthesis ◽  
Glucose Production ◽  
Receptor Expression ◽  
Acid Uptake

The liver is one of the most essential organs involved in the regulation of energy homeostasis. Hepatic steatosis, a major manifestation of metabolic syndrome, is associated with imbalance between lipid formation and breakdown, glucose production and catabolism, and cholesterol synthesis and secretion. Epidemiological studies show sex difference in the prevalence in fatty liver disease and suggest that sex hormones may play vital roles in regulating hepatic steatosis. In this review, we summarize current literature and discuss the role of estrogens and androgens and the mechanisms through which estrogen receptors and androgen receptors regulate lipid and glucose metabolism in the liver. In females, estradiol regulates liver metabolism via estrogen receptors by decreasing lipogenesis, gluconeogenesis, and fatty acid uptake, while enhancing lipolysis, cholesterol secretion, and glucose catabolism. In males, testosterone works via androgen receptors to increase insulin receptor expression and glycogen synthesis, decrease glucose uptake and lipogenesis, and promote cholesterol storage in the liver. These recent integrated concepts suggest that sex hormone receptors could be potential promising targets for the prevention of hepatic steatosis.

scholarly journals Molecular Investigation of Brain Tumors Progressing During Pregnancy or Postpartum Period: The Association Between Tumor Type, Their Receptors, and the Timing of Presentation

2021 ◽  
Author(s):  
Saeko Ichimura ◽  
Kentaro Ohara ◽  
Maya Kono ◽  
Katsuhiro Mizutani ◽  
Yohei Kitamura ◽  
...  
Keyword(s):  
Growth Factors ◽  
Brain Tumors ◽  
Sex Hormones ◽  
Postpartum Period ◽  
Hormone Receptors ◽  
Receptor Expression ◽  
Vestibular Schwannomas ◽  
Comparative Genomic ◽  
Tumor Type ◽  
Her 2

Abstract Brain tumors are frequently present during pregnancy; however, the mechanism has not been well elucidated. Purpose of this study is to investigate the influence of molecular genetic factors on the progression of brain tumors during pregnancy or the postpartum period. Twelve cases of brain tumors that presented during pregnancy or postpartum period were included: five gliomas, three meningiomas, two vestibular schwannomas, and two chordomas. Tumor samples were investigated by metaphase comparative genomic hybridization and immunohistochemistry, for chromosomal copy number aberration (CNA) and receptor expression of sex hormones and growth factors. The results were correlated with the timing of tumor presentation in relation to the stage of pregnancy. EGFR, VEGFR-1/2, AR, and c-Myc were expressed in gliomas, PgR, ER, HER-2, VEGFR-1, EGF and VEGFR2 in meningiomas, VEGFR-1 in vestibular schwannomas, and EGFR, VEGFR-1/2, and c-Myc in chordomas. The CNAs of the tumors varied. Four of the five gliomas presented in the 2nd trimester, all three meningiomas in the 3rd trimester or postpartum period, and both of the two schwannomas in the late 2nd trimester. Expression of VEGFR-1/2 and EGFR was observed regardless of the timing of tumor presentation, whereas female hormone receptors and HER-2 were exclusively found in meningiomas. Interestingly, one anaplastic astrocytoma (IDH mut, non-codeleted) that progressed from precedent grade 2 tumor harbored amplification of the MYC locus. Progression of brain tumors during pregnancy is associated with various growth factors as well as sex hormones. The timing of presentation is likely dependent on molecular　receptors specific to each tumor type.

Embryonic steroids control developmental programming of energy balance

Endocrinology ◽  
2021 ◽  
Author(s):  
Meng-Chun Monica Shih ◽  
Chen-Che Jeff Huang ◽  
Hsueh-Ping Chu ◽  
Nai-Chi Hsu ◽  
Bon-chu Chung
Keyword(s):  
Energy Source ◽  
Blood Glucose ◽  
Energy Homeostasis ◽  
De Novo ◽  
Glycogen Synthesis ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Expression Of Genes ◽  
Major Energy Source

Abstract Glucose is a major energy source for growth. At birth, neonates must change their energy source from maternal supply to its own glucose production. The mechanism of this transition has not been clearly elucidated. To evaluate the possible roles of steroids in this transition, here we examine the defects associated with energy production of a mouse line that cannot synthesize steroids de novo due to the disruption of its Cyp11a1 gene. The Cyp11a1 null embryos had insufficient blood insulin, and failed to store glycogen in the liver since embryonic day 16.5. Their blood glucose dropped soon after maternal deprivation, and the expression of hepatic gluconeogenic and glycogenic genes were reduced. Insulin was synthesized in the mutant fetal pancreas, but failed to be secreted. Maternal glucocorticoid supply rescued the amounts of blood glucose, insulin, and liver glycogen in the fetus, but did not restore expression of genes for glycogen synthesis, indicating the requirement of de novo glucocorticoid synthesis for glycogen storage. Thus, our investigation of Cyp11a1 null embryos reveals that the energy homeostasis is established before birth, and fetal steroids are required for the regulation of glycogen synthesis, hepatic gluconeogenesis and insulin secretion at the fetal stage.

scholarly journals Hepatic Overexpression of CD36 Improves Glycogen Homeostasis and Attenuates High-Fat Diet-Induced Hepatic Steatosis and Insulin Resistance

2016 ◽  
Vol 36 (21) ◽  
pp. 2715-2727 ◽  
Author(s):  
Wojciech G. Garbacz ◽  
Peipei Lu ◽  
Tricia M. Miller ◽  
Samuel M. Poloyac ◽  
Nicholas S. Eyre ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Glycogen Synthesis ◽  
Metabolic Stress ◽  
Density Lipoprotein ◽  
Fatty Acid Uptake ◽  
Arachidonic Acid Metabolite ◽  
Acid Uptake ◽  
High Fat

The common complications in obesity and type 2 diabetes include hepatic steatosis and disruption of glucose-glycogen homeostasis, leading to hyperglycemia. Fatty acid translocase (FAT/CD36), whose expression is inducible in obesity, is known for its function in fatty acid uptake. Previous work by us and others suggested that CD36 plays an important role in hepatic lipid homeostasis, but the results have been conflicting and the mechanisms were not well understood. In this study, by using CD36-overexpressing transgenic (CD36Tg) mice, we uncovered a surprising function of CD36 in regulating glycogen homeostasis. Overexpression of CD36 promoted glycogen synthesis, and as a result, CD36Tg mice were protected from fasting hypoglycemia. When challenged with a high-fat diet (HFD), CD36Tg mice showed unexpected attenuation of hepatic steatosis, increased very low-density lipoprotein (VLDL) secretion, and improved glucose tolerance and insulin sensitivity. The HFD-fed CD36Tg mice also showed decreased levels of proinflammatory hepatic prostaglandins and 20-hydroxyeicosatetraenoic acid (20-HETE), a potent vasoconstrictive and proinflammatory arachidonic acid metabolite. We propose that CD36 functions as a protective metabolic sensor in the liver under lipid overload and metabolic stress. CD36 may be explored as a valuable therapeutic target for the management of metabolic syndrome.

1870-P: Glucagon-Receptor Signaling Reverses Hepatic Steatosis Independent of Leptin Receptor Expression

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1870-P
Author(s):  
SHELLY NASON ◽  
TEAYOUN KIM ◽  
JESSICA P. ANTIPENKO ◽  
BRIAN FINAN ◽  
RICHARD DIMARCHI ◽  
...  
Keyword(s):  
Hepatic Steatosis ◽  
Leptin Receptor ◽  
Receptor Expression ◽  
Receptor Signaling ◽  
Glucagon Receptor

Role of sex hormones in lung cancer

2021 ◽  
pp. 153537022110196
Author(s):  
Nathalie Fuentes ◽  
Miguel Silva Rodriguez ◽  
Patricia Silveyra
Keyword(s):  
Lung Cancer ◽  
Sex Differences ◽  
Sex Hormones ◽  
Hormone Receptors ◽  
Occupational Exposures ◽  
Lung Carcinogenesis ◽  
Male And Female ◽  
Female Sex ◽  
Incidence And Mortality ◽  
Cancer Rates

Lung cancer represents the world’s leading cause of cancer deaths. Sex differences in the incidence and mortality rates for various types of lung cancers have been identified, but the biological and endocrine mechanisms implicated in these disparities have not yet been determined. While some cancers such as lung adenocarcinoma are more commonly found among women than men, others like squamous cell carcinoma display the opposite pattern or show no sex differences. Associations of tobacco product use rates, susceptibility to carcinogens, occupational exposures, and indoor and outdoor air pollution have also been linked to differential rates of lung cancer occurrence and mortality between sexes. While roles for sex hormones in other types of cancers affecting women or men have been identified and described, little is known about the influence of sex hormones in lung cancer. One potential mechanism identified to date is the synergism between estrogen and some tobacco compounds, and oncogene mutations, in inducing the expression of metabolic enzymes, leading to enhanced formation of reactive oxygen species and DNA adducts, and subsequent lung carcinogenesis. In this review, we present the literature available regarding sex differences in cancer rates, associations of male and female sex hormones with lung cancer, the influence of exogenous hormone therapy in women, and potential mechanisms mediated by male and female sex hormone receptors in lung carcinogenesis. The influence of biological sex on lung disease has recently been established, thus new research incorporating this variable will shed light on the mechanisms behind the observed disparities in lung cancer rates, and potentially lead to the development of new therapeutics to treat this devastating disease.

scholarly journals The Neuronal Actions of Leptin and the Implications for Treating Alzheimer’s Disease

2021 ◽  
Vol 14 (1) ◽  
pp. 52
Author(s):  
Kirsty Hamilton ◽  
Jenni Harvey
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Energy Homeostasis ◽  
Leptin Receptor ◽  
Hippocampal Formation ◽  
Synaptic Function ◽  
Receptor Expression ◽  
Neuroprotective Actions ◽  
Novel Target ◽  
Leptin System

It is widely accepted that the endocrine hormone leptin controls food intake and energy homeostasis via activation of leptin receptors expressed on hypothalamic arcuate neurons. The hippocampal formation also displays raised levels of leptin receptor expression and accumulating evidence indicates that leptin has a significant impact on hippocampal synaptic function. Thus, cellular and behavioural studies support a cognitive enhancing role for leptin as excitatory synaptic transmission, synaptic plasticity and glutamate receptor trafficking at hippocampal Schaffer collateral (SC)-CA1 synapses are regulated by leptin, and treatment with leptin enhances performance in hippocampus-dependent memory tasks. Recent studies indicate that hippocampal temporoammonic (TA)-CA1 synapses are also a key target for leptin. The ability of leptin to regulate TA-CA1 synapses has important functional consequences as TA-CA1 synapses are implicated in spatial and episodic memory processes. Moreover, degeneration is initiated in the TA pathway at very early stages of Alzheimer’s disease, and recent clinical evidence has revealed links between plasma leptin levels and the incidence of Alzheimer’s disease (AD). Additionally, accumulating evidence indicates that leptin has neuroprotective actions in various AD models, whereas dysfunctions in the leptin system accelerate AD pathogenesis. Here, we review the data implicating the leptin system as a potential novel target for AD, and the evidence that boosting the hippocampal actions of leptin may be beneficial.

scholarly journals High consistency between characteristics of primary intraductal breast cancer and subtype of subsequent ipsilateral invasive cancer

2019 ◽  
Vol 106 (1) ◽  
pp. 64-69
Author(s):  
Massimiliano Gennaro ◽  
Elisabetta Meneghini ◽  
Paolo Baili ◽  
Sara Bravaccini ◽  
Annalisa Curcio ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Active Surveillance ◽  
Hormone Receptors ◽  
Ductal Carcinoma ◽  
Tumor Grade ◽  
Receptor Expression ◽  
Invasive Cancer ◽  
Her2 Positive ◽  
Hormone Receptor Expression ◽  
High Consistency

Background: Ductal carcinoma in situ (DCIS) is considered a morphologic precursor of invasive cancer and is often treated with adjuvant whole-breast irradiation and endocrine therapy, as if it were an invasive cancer. Our aim was to provide further support for treatment de-escalation or enrollment of such patients in active surveillance trials. Methods: We retrospectively analyzed data on patients with conservatively treated primary DCIS subsequently diagnosed with ipsilateral invasive breast cancer (IBC) at 2 comprehensive breast cancer centers. From their merged databases, we identified 50 cases with full details on tumor grade, hormone receptor expression, and HER2 amplification, for both the primary DCIS and the corresponding IBC, and we assessed the similarities and differences between the two. Results: Distributions of hormone receptors were similar in primary DCIS and IBC, while high-grade and HER2-positive status was less common in IBC than in primary DCIS. The positivity for estrogen receptors (ER) and well-differentiated or moderately differentiated morphology in the primary DCIS persisted in 90% of the matching IBC. Changes in progesterone receptor expression were slightly more common than those in ER expression. Overall consistency for the luminal-like receptors subtype was found in 90% of cases. Conclusion: The high consistency between the features of primary DCIS and those of subsequent IBC (in the rare but not negligible cases of local failure) should be borne in mind when considering the therapeutic options. Treatment de-escalation and accrual of patients for active surveillance trials could be appropriate for luminal-like precursors.

Cannabinoid receptor expression in the placenta and their potential role in energy homeostasis signalling

Placenta ◽  
2021 ◽  
Vol 112 ◽  
pp. e73
Author(s):  
Birgit Hirschmugl ◽  
Johanna Wachutka ◽  
Sandra Meitz ◽  
Karl Tamussino ◽  
Christian Wadsack
Keyword(s):  
Energy Homeostasis ◽  
Potential Role ◽  
Cannabinoid Receptor ◽  
Receptor Expression

scholarly journals Inhibition of glycogenolysis enhances gluconeogenic precursor uptake by the liver of conscious dogs

1997 ◽  
Vol 273 (5) ◽  
pp. E868-E879 ◽  
Author(s):  
Masakazu Shiota ◽  
Patricia A. Jackson ◽  
Hilmar Bischoff ◽  
Michael McCaleb ◽  
Melanie Scott ◽  
...  
Keyword(s):  
Glycogen Synthesis ◽  
Control Period ◽  
Glucose Production ◽  
Hepatic Uptake ◽  
Endogenous Glucose Production ◽  
Conscious Dogs ◽  
Intragastric Administration ◽  
Endogenous Insulin ◽  
Glucose Output ◽  
Gluconeogenic Substrates

We investigated the effect of inhibiting glycogenolysis on gluconeogenesis in 18-h-fasted conscious dogs with the use of intragastric administration of BAY R 3401, a glycogen phosphorylase inhibitor. Isotopic ([3-3H]glucose and [U-14C]alanine) and arteriovenous difference methods were used to assess glucose metabolism. Each study consisted of a 100-min equilibration, a 40-min control, and two 90-min test periods. Endogenous insulin and glucagon secretions were inhibited with somatostatin (0.8 μg ⋅ kg−1 ⋅ min−1), and the two hormones were replaced intraportally (insulin: 0.25 mU ⋅ kg−1 ⋅ min−1; glucagon: 0.6 ng ⋅ kg−1 ⋅ min−1). Drug (10 mg/kg) or placebo was given after the control period. Insulin and glucagon were kept at basal levels in the first test period, after which glucagon infusion was increased to 2.4 ng ⋅ kg−1 ⋅ min−1; BAY R 3401 decreased tracer-determined endogenous glucose production [rate of glucose production (Ra): 14 ± 1 to 7 ± 1 μmol ⋅ kg−1 ⋅ min−1] and net hepatic glucose output (11 ± 1 to 3 ± 2 μmol ⋅ kg−1 ⋅ min−1) during test 1. It increased the net hepatic uptake of gluconeogenic substrates from 9.0 ± 2.0 to 11.6 ± 0.6 μmol ⋅ kg−1 ⋅ min−1. Basal glycogenolysis was decreased by drug (9.1 ± 0.7 to 1.5 ± 0.2 μmol glucosyl U ⋅ kg−1 ⋅ min−1). Placebo had no effect on Ra or the uptake of gluconeogenic precursors by the liver. The rise in glucagon increased Ra by 22 ± 3 and by 8 ± 2 μmol ⋅ kg−1 ⋅ min−1(at 10 min) in placebo and drug, respectively. The rise in glucagon caused little change in the net hepatic uptake (μmol ⋅ kg−1 ⋅ min−1) of gluconeogenic substrates in placebo (8.2 ± 0.6 to 9.0 ± 1.0) but increased it markedly (11.6 ± 0.6 to 15.4 ± 1.0) in drug. Glucagon increased glycogenolysis by 22.1 ± 2.5 and by 7.8 ± 1.6 μmol ⋅ kg−1 ⋅ min−1in placebo and drug, respectively. The amount of glycogen (μmol glucosyl U/kg) synthesized from gluconeogenic carbon was four times higher in drug (48.6 ± 9.7) than in placebo (11.3 ± 1.7). We conclude that BAY R 3401 caused a marked reduction in basal and glucagon-stimulated glycogenolysis. As a result of these changes, there was an increase in the net hepatic uptake of gluconeogenic precursors and in glycogen synthesis.

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