scholarly journals Gender-Specific Expression and Mechanism of Regulation of Estrogen Sulfotransferase in Adipose Tissues of the Mouse

Endocrinology ◽  
2008 ◽  
Vol 149 (11) ◽  
pp. 5440-5448 ◽  
Author(s):  
Victor K. Khor ◽  
Ming Han Tong ◽  
Yueming Qian ◽  
Wen-Chao Song
Keyword(s):  
Female Mouse ◽  
Male Mice ◽  
Estrogen Sulfotransferase ◽  
Specific Expression ◽  
Adipose Tissues ◽  
Testosterone Treatment ◽  
Female Mice ◽  
Fat Depots ◽  
Epididymal Fat ◽  
Gender Specific

Although primarily regarded as a sex steroid, estrogen plays an important role in many other physiological processes including adipose development and disposition. Estrogen sulfotransferase (EST) regulates estrogen activity by catalyzing the sulfoconjugation and inactivation of estrogens. In the present study, we report the gender-specific expression of EST in adipose tissues of the mouse and describe contrasting mechanisms of EST regulation in the fat and liver. EST is expressed in the white adipose tissues of the male but not female mouse. Within the various fat depots of male mice, it is most abundantly expressed in the epididymal fat pad, with variable levels in other white fats and no expression in the brown fat. Fractionation of epididymal fat cells showed EST to be predominantly associated with stromal vascular cells (preadipocyte). EST expression in male mouse adipose tissues is dependent on testosterone as castration ablated, and administration of exogenous testosterone restored, EST expression. Furthermore, testosterone treatment induced abnormal EST expression in the parametrial fat of female mice. EST induction by testosterone in female mice is tissue specific because testosterone treatment had no effect on liver EST expression. Conversely, the liver X receptor agonist TO-901317 induced EST expression in female mouse liver but not in their adipose tissues. Finally, we demonstrate that male EST knockout mice developed increased epididymal fat accumulation with enlarged adipocyte size. We conclude that EST is expressed in adipose tissues in a sexually dimorphic manner, is regulated by testosterone, and plays a physiological role in regulating adipose tissue accumulation in male mice.

scholarly journals Adipocyte-specific modulation of KLF14 expression in mice leads to sex-dependent impacts in adiposity and lipid metabolism

2021 ◽  
Author(s):  
Qianyi Yang ◽  
Jameson Hinkle ◽  
Jordan N Reed ◽  
Redouane Aherrahrou ◽  
Zhiwen Xu ◽  
...  
Keyword(s):  
Fat Mass ◽  
Risk Allele ◽  
Lipid Storage ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Male Mice ◽  
Adipose Tissues ◽  
Female Mice ◽  
Fat Depots ◽  
Deficient Mice

Genome-wide association studies identified single nucleotide polymorphisms on chromosome 7 upstream of KLF14 to be associated with metabolic syndrome traits and increased risk for Type 2 Diabetes (T2D). The associations were more significant in women than in men. The risk allele carriers expressed lower levels of the transcription factor KLF14 in adipose tissues than non-risk allele carriers. To investigate how adipocyte KLF14 regulates metabolic traits in a sex-dependent manner, we characterized high-fat diet fed male and female mice with adipocyte-specific Klf14 deletion or overexpression. Klf14 deletion resulted in increased fat mass in female mice and decreased fat mass in male mice. Female Klf14-deficient mice had overall smaller adipocytes in subcutaneous fat depots but larger adipocytes in parametrial depots, indicating a shift in lipid storage from subcutaneous to visceral fat depots. They had reduced metabolic rates and increased respiratory exchange ratios consistent with increased utilization of carbohydrates as an energy source. Fasting and isoproterenol-induced adipocyte lipolysis was defective in female Klf14-deficient mice and concomitantly adipocyte triglycerides lipase mRNA levels were downregulated. Female Klf14-deficient mice cleared blood triglyceride and NEFA less efficiently than wild type. Finally, adipocyte-specific overexpression of Klf14 resulted in lower total body fat in female but not male mice. Taken together, consistent with human studies, adipocyte KLF14 deficiency in female but not in male mice causes increased adiposity and redistribution of lipid storage from subcutaneous to visceral adipose tissues. Increasing KLF14 abundance in adipocytes of females with obesity and T2D may provide a novel treatment option to alleviate metabolic abnormalities.

Lethal factor released from submandibular grafts in mice

1969 ◽  
Vol 47 (4) ◽  
pp. 329-334 ◽  
Author(s):  
K. Hoshino ◽  
C. D. Lin
Keyword(s):  
Submandibular Gland ◽  
Female Mouse ◽  
Lethal Factor ◽  
Lethal Effect ◽  
Mature Female ◽  
Male Mice ◽  
Normal Organ ◽  
Female Mice ◽  
Immature Male ◽  
Series Of Experiments

The present series of experiments clearly demonstrates the existence of the lethal factor in the submandibular gland of male BALB/c mice. This lethal factor was released from the submandibular gland of male mice when the glands were transplanted autologously into submandibular-sialoadenectomized male mice or isologously into normal intact adult male or female mice. Neither the sublingual nor the parotid grafts demonstrated the same effect. The lethal effect was not observed in the experiments with submandibular grafts obtained from immature male or mature female mice. As a host, the female mouse was found to be more susceptible to the lethal factor. There was a linear relationship between the strength of the lethal factor and the number of submandibular grafts used. The site of production of the lethal factor is unknown. It was extremely unusual to see the death of host mice which merely received a normal organ other than the submandibular gland.

The influence of pituitary and gonadal hormones on serum levels of pregnancy-associated murine protein-1

1983 ◽  
Vol 104 (1) ◽  
pp. 23-26 ◽  
Author(s):  
J. Hau ◽  
A. A. Gidley-Baird ◽  
B. Teisner ◽  
P. Svendsen ◽  
J. G. Westergaard
Keyword(s):  
Adult Male ◽  
Serum Levels ◽  
Gonadal Hormones ◽  
Male Mice ◽  
Testosterone Treatment ◽  
Female Mice

Abstract. Hypophysectomy of female mice resulted in the disappearance of pregnancy-associated murine protein-1 (PAMP-1) from the circulation within a week. Maintenance of physiological levels of oestrogen, progesterone, testosterone, LH, FSH or prolactin was not sufficient to maintain a normal PAMP-1 level in the hypophysectomized animals. However, administration of oestrogen in large doses to adult male mice with undectable levels of circulating PAMP-1 caused PAMP-1 to appear in the blood. Testosterone treatment of females inhibited the PAMP-1 synthesis.

scholarly journals Sex Difference in Corticosterone-Induced Insulin Resistance in Mice

Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2367-2387 ◽  
Author(s):  
Kasiphak Kaikaew ◽  
Jacobie Steenbergen ◽  
Theo H van Dijk ◽  
Aldo Grefhorst ◽  
Jenny A Visser
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Prolonged Exposure ◽  
Morphological Changes ◽  
Elevated Serum ◽  
High Dose ◽  
Dependent Manner ◽  
Male Mice ◽  
Adipose Tissues ◽  
Female Mice

Abstract Prolonged exposure to glucocorticoids (GCs) causes various metabolic derangements. These include obesity and insulin resistance, as inhibiting glucose utilization in adipose tissues is a major function of GCs. Although adipose tissue distribution and glucose homeostasis are sex-dependently regulated, it has not been evaluated whether GCs affect glucose metabolism and adipose tissue functions in a sex-dependent manner. In this study, high-dose corticosterone (rodent GC) treatment in C57BL/6J mice resulted in nonfasting hyperglycemia in male mice only, whereas both sexes displayed hyperinsulinemia with normal fasting glucose levels, indicative of insulin resistance. Metabolic testing using stable isotope-labeled glucose techniques revealed a sex-specific corticosterone-driven glucose intolerance. Corticosterone treatment increased adipose tissue mass in both sexes, which was reflected by elevated serum leptin levels. However, female mice showed more metabolically protective adaptations of adipose tissues than did male mice, demonstrated by higher serum total and high-molecular-weight adiponectin levels, more hyperplastic morphological changes, and a stronger increase in mRNA expression of adipogenic differentiation markers. Subsequently, in vitro studies in 3T3-L1 (white) and T37i (brown) adipocytes suggest that the increased leptin and adiponectin levels were mainly driven by the elevated insulin levels. In summary, this study demonstrates that GC-induced insulin resistance is more severe in male mice than in female mice, which can be partially explained by a sex-dependent adaptation of adipose tissues.

K+-dependent Na+/Ca2+ exchanger 3 is involved in renal active calcium transport and is differentially expressed in the mouse kidney

2009 ◽  
Vol 297 (2) ◽  
pp. F371-F379 ◽  
Author(s):  
Geun-Shik Lee ◽  
Kyung-Chul Choi ◽  
Eui-Bae Jeung
Keyword(s):  
Calcium Transport ◽  
Critical Role ◽  
Mature Female ◽  
Differentially Expressed ◽  
Male Mice ◽  
Specific Expression ◽  
Female Mice ◽  
Calcium Reabsorption ◽  
Active Calcium ◽  
Convoluted Tubules

Previously, we reported that renal active calcium-transporting genes are highly expressed in female mice and suggested that renal calcium-processing genes play a critical role in normal calcium reabsorption in females (Lee GS, Lee KY, Choi KC, Ryu YH, Paik SG, Oh GT, Jeung EB. J Bone Miner Res 22: 1968–1978, 2007). In the current study, we evaluated the differential expression of renal calcium-processing genes in male and female mice. Using microarray analysis, we identified K+-dependent Na+/Ca2+ exchanger 3 ( NCKX3) as a gene that was differentially expressed in the kidneys of female and male mice. The expression levels of renal NCKX3 mRNA and protein were higher in female than in male mice, whereas there was no difference between the genders in the levels of NCKX3 expression in the brain. Renal NCKX3 localized to the basolateral layer of distal convoluted tubules, indicating that this protein participates in renal calcium reabsorption. To identify putative regulators in the gender-specific expression of NCKX3, several hormones were injected into mature female and male mice. Although any hormones did not alter NCKX3 expression, adrenal gland-secreted hormones aldosterone and hydrocortisone did downregulate renal NCKX3 mRNA expression in female mice, but they did not change its protein levels. Taken together, the results in this study suggest that a high level of renal NCKX3 expression maintain in distal convoluted tubules may play a role in active calcium transport in the kidneys of female mice.

scholarly journals Inhibition of Estrogen Sulfotransferase (SULT1E1/EST) Ameliorates Ischemic Acute Kidney Injury in Mice

2020 ◽  
Vol 31 (7) ◽  
pp. 1496-1508
Author(s):  
Anne C. Silva Barbosa ◽  
Dong Zhou ◽  
Yang Xie ◽  
You-Jin Choi ◽  
Hung-Chun Tung ◽  
...  
Keyword(s):  
Knockout Mice ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Male Mice ◽  
Wild Type ◽  
Estrogen Sulfotransferase ◽  
Female Mice ◽  
Pharmacologic Inhibition

BackgroundStudies have suggested that estrogens may protect mice from AKI. Estrogen sulfotransferase (SULT1E1, or EST) plays an important role in estrogen homeostasis by sulfonating and deactivating estrogens, but studies on the role of SULT1E1 in AKI are lacking.MethodsWe used the renal ischemia-reperfusion model to investigate the role of SULT1E1 in AKI. We subjected wild-type mice, Sult1e1 knockout mice, and Sult1e1 knockout mice with liver-specific reconstitution of SULT1E1 expression to bilateral renal ischemia-reperfusion or sham surgery, either in the absence or presence of gonadectomy. We assessed relevant biochemical, histologic, and gene expression markers of kidney injury. We also used wild-type mice treated with the SULT1E1 inhibitor triclosan to determine the effect of pharmacologic inhibition of SULT1E1 on AKI.ResultsAKI induced the expression of Sult1e1 in a tissue-specific and sex-specific manner. It induced expression of Sult1e1 in the liver in both male and female mice, but Sult1e1 induction in the kidney occurred only in male mice. Genetic knockout or pharmacologic inhibition of Sult1e1 protected mice of both sexes from AKI, independent of the presence of sex hormones. Instead, a gene profiling analysis indicated that the renoprotective effect was associated with increased vitamin D receptor signaling. Liver-specific transgenic reconstitution of SULT1E1 in Sult1e1 knockout mice abolished the protection in male mice but not in female mice, indicating that Sult1e1’s effect on AKI was also tissue-specific and sex-specific.ConclusionsSULT1E1 appears to have a novel function in the pathogenesis of AKI. Our findings suggest that inhibitors of SULT1E1 might have therapeutic utility in the clinical management of AKI.

Dexamethasone-induced hyperglycemia in obese Avy/a (viable yellow) female mice entails preferential induction of a hepatic estrogen sulfotransferase

Diabetes ◽  
1994 ◽  
Vol 43 (8) ◽  
pp. 999-1004 ◽  
Author(s):  
A. M. Gill ◽  
E. H. Leiter ◽  
J. G. Powell ◽  
H. D. Chapman ◽  
T. T. Yen
Keyword(s):  
Estrogen Sulfotransferase ◽  
Female Mice ◽  
Yellow Female

Gender-Specific Expression of Arginine-Vasotocin in the Chicken Brain

2004 ◽  
Vol 15 (3) ◽  
pp. 219-223 ◽  
Author(s):  
R. Grossmann ◽  
A. Jurkevich ◽  
S. Klein
Keyword(s):  
Arginine Vasotocin ◽  
Specific Expression ◽  
Chicken Brain ◽  
Gender Specific

scholarly journals Expression of type one cannabinoid receptor in different subpopulation of kisspeptin neurons and kisspeptin afferents to GnRH neurons in female mice

2021 ◽  
Author(s):  
Tamás Wilheim ◽  
Krisztina Nagy ◽  
Mahendravarman Mohanraj ◽  
Kamil Ziarniak ◽  
Masahiko Watanabe ◽  
...  
Keyword(s):  
Cannabinoid Receptor ◽  
Third Ventricle ◽  
Glutamate Transporter ◽  
Neuroendocrine Cells ◽  
Receptor Protein ◽  
Specific Expression ◽  
Female Mice ◽  
Gnrh Neurons ◽  
Periventricular Area ◽  
Cycle Dependent

AbstractThe endocannabinoids have been shown to target the afferents of hypothalamic neurons via cannabinoid 1 receptor (CB1) and thereby to influence their excitability at various physiological and/or pathological processes. Kisspeptin (KP) neurons form afferents of multiple neuroendocrine cells and influence their activity via signaling through a variation of co-expressed classical neurotransmitters and neuropeptides. The differential potency of endocannabinoids to influence the release of classical transmitters or neuropeptides, and the ovarian cycle-dependent functioning of the endocannabinoid signaling in the gonadotropin-releasing hormone (GnRH) neurons initiated us to study whether (a) the different subpopulations of KP neurons express CB1 mRNAs, (b) the expression is influenced by estrogen, and (c) CB1-immunoreactivity is present in the KP afferents to GnRH neurons. The aim of the study was to investigate the site- and cell-specific expression of CB1 in female mice using multiple labeling in situ hybridization and immunofluorescent histochemical techniques. The results support that CB1 mRNAs are expressed by both the GABAergic and glutamatergic subpopulations of KP neurons, the receptor protein is detectable in two-thirds of the KP afferents to GnRH neurons, and the expression of CB1 mRNA shows an estrogen-dependency. The applied estrogen-treatment, known to induce proestrus, reduced the level of CB1 transcripts in the rostral periventricular area of the third ventricle and arcuate nucleus, and differently influenced its co-localization with vesicular GABA transporter or vesicular glutamate transporter-2 in KP neurons. This indicates a gonadal cycle-dependent role of endocannabinoid signaling in the neuronal circuits involving KP neurons.

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