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Mashup Score: 0Glucagon-like peptide-1 analog, liraglutide, regulates Sertoli cell energy metabolism - 6 hour(s) ago
Liraglutide, an analog of the incretin hormone glucagon-like peptide 1 (GLP-1), is widely used for obesity and type 2 diabetes treatment. However, there is scarce information about its effects on testicular function. Within the testis, Sertoli cells (SCs) provide nutritional support for germ cells; they metabolize glucose to lactate, which is delivered to germ cells to be used as a preferred energy substrate. Besides, SCs use fatty acids (FAs) as an energy source and store them as triacylglycerols (TAGs) within lipid droplets (LDs), which serve as an important energy reserve. In the present study, 20-day-old rat SC cultures were used to assess whether liraglutide affects their metabolic functions related to nutritional support and lipid storage. The results show that liraglutide does not modify glucose consumption or lactate production. However, it increases TAG levels and LD content. These effects are accompanied by an increase in the mRNA levels of the fatty acid transporter FAT/CD36
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet
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Mashup Score: 5
Systemic glucocorticoid excess causes several adverse metabolic conditions, most notably Cushing’s syndrome. These effects are amplified by the intracellular enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Here, we determined the less well-characterised effects of glucocorticoid excess, and the contribution of 11β-HSD1 amplification on metabolic rate in mice. Male and female C57BL/6J (wild type, WT) and 11β-HSD1 knockout (11β-HSD1 KO) mice were treated with high-dose corticosterone or a vehicle control for 3 weeks. Indirect calorimetry was conducted during the final week of treatment, with or without fasting, to determine the impact on metabolic rate. We found that corticosterone treatment elevated metabolic rate and promoted carbohydrate utilisation primarily in female WT mice, with effects more pronounced during the light phase. Corticosterone treatment also resulted in greater fat accumulation in female WT mice. Corticosterone induced hyperphagia was identified as a likel
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet-
In this study Samuel R Heaselgrave et al. determined the less well-characterised effects of #glucocorticoid excess, and the contribution of 11β-HSD1 amplification on #metabolic rate in mice. Read it here 👉 https://t.co/qxcD1qx8Fz @UTSWMedCenter @unibirmingham @NottmTrentUni https://t.co/Yw3xDFFGxm
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Mashup Score: 2Sex Effects in Endocrine Health and Disease - 25 day(s) ago
Journal of Endocrinology special collection titled Sex Effects in Endocrine Health and Disease
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet-
📢 NEW special collection: Sex Effects in Endocrine Health and Disease We welcome for submission studies which highlight both convergent and divergent responses in males and females, focusing on basic and translational science. Learn more: https://t.co/ULgLRoBoSF https://t.co/VKXSfRe6ts
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Mashup Score: 1Sex Effects in Endocrine Health and Disease - 2 month(s) ago
Journal of Endocrinology special collection titled Sex Effects in Endocrine Health and Disease
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet-
📢 NEW special collection: Sex Effects in Endocrine Health and Disease We welcome for submission studies which highlight both convergent and divergent responses in males and females, focusing on basic and translational science. Learn more: https://t.co/ULgLRoBoSF https://t.co/VKXSfRe6ts
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Mashup Score: 1
Aldosterone is a mineralocorticoid hormone involved in controlling electrolyte balance, blood pressure, and cellular signaling. It plays a pivotal role in cardiovascular and metabolic physiology. Excess aldosterone activates mineralocorticoid receptors, leading to subsequent inflammatory responses, increased oxidative stress, and tissue remodeling. Various mechanisms have been reported to link aldosterone with cardiovascular and metabolic diseases. However, mitochondria, responsible for energy generation through oxidative phosphorylation, have received less attention regarding their potential role in aldosterone-related pathogenesis. Excess aldosterone leads to mitochondrial dysfunction, and this may play a role in the development of cardiovascular and metabolic diseases. Aldosterone has the potential to affect mitochondrial structure, function, and dynamic processes, such as mitochondrial fusion and fission. In addition, aldosterone has been associated with the suppression of mitochon
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet-
Cheng-Hsuan Tsai et al. explore the mechanisms underlying #aldosterone-induced #cardiovascular and #metabolic #mitochondrial dysfunction, including mineralocorticoid receptor activation and subsequent inflammatory responses. Read it here ➡️ https://t.co/rSo8j4mfQe https://t.co/HqJrGslwy9
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Mashup Score: 0miR-181d-5p ameliorates hypercholesterolemia by targeting PCSK9 - 2 month(s) ago
Hypercholesterolemia is an independent risk factor for cardiovascular disease and lowering circulating levels of low-density lipoprotein cholesterol (LDL-C) can prevent and reduce cardiovascular events. MicroRNA-181d (miR-181d) can reduce the levels of triglycerides and cholesterol esters in cells. However, it is not known whether miR-181d-5p can lower levels of circulating LDL-C. Here, we generated two animal models of hypercholesterolemia to analyze the potential relationship between miR-181d-5p and LDL-C. In hypercholesterolemia model mice, adeno-associated virus (AAV)-mediated liver-directed overexpression of miR-181d-5p decreased the serum levels of cholesterol and LDL-C and the levels of cholesterol and triglyceride in the liver compared with control mice. Target Scan 8.0 indicated Proprotein convertase subtilisin/kexin type 9 (PCSK9) to be a possible target gene of miR-181d-5p, which was confirmed by in vitro experiments. miR-181d-5p could directly interact with both the PCSK9 3
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet-
A recent study by Yu Wang et al. that found the expression of miR-181d-5p was increased in the livers of #hypercholesterolemia model mice and hamsters. Read the #openaccess article 👉 https://t.co/WcLimrTuTn https://t.co/eoWf96u5jt
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Mashup Score: 7Editorial Board - 2 month(s) ago
Joint JOE and JME international editorial board
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet-
We are delighted to welcome Dr Minna Woo to our Editorial Board as Diabetes Senior Editor. @woo_minna is Director of the Banting and Best Diabetes Centre at University of Toronto @BBDC_UofT, and clinician scientist & Professor @UofTmedicine. Learn more 👉 https://t.co/uaIKwZJNjw https://t.co/z0WOEz89xJ
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Mashup Score: 2
Ghrelin has effects that range from the maturation of the central nervous system to the regulation of energy balance. The production of ghrelin increases significantly during the first weeks of life. Studies have addressed the metabolic effects of liver-expressed antimicrobial peptide 2 (LEAP2) in inhibiting the effects evoked by ghrelin, mainly in glucose homeostasis, insulin resistance, and lipid metabolism. Despite the known roles of ghrelin in the postnatal development, little is known about the long-term metabolic influences of modulation with the endogenous expressed growth hormone secretagogue receptor (GHSR) inverse agonist LEAP2. This study aimed to evaluate the contribution of GHSR signalling during perinatal phases, to neurodevelopment and energy metabolism in young animals, under inverse antagonism by LEAP2[1–14]. For this, two experimental models were used: (i) LEAP2[1–14] injections in female rats during the pregnancy. (ii) Postnatal modulation of GHSR with LEAP2[1–14] or
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet-
Marcos Divino Ferreira-Junior et al. sought to understand the role of growth hormone secretagogue receptor (GHSR) signalling in the evolution of body weight and energy metabolism in young rats exposed early in life to #GHSR modulators. Read their study 👉 https://t.co/AwW79a8Q5O https://t.co/lz3OuhwJ0G
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Mashup Score: 2Bidirectional crosstalk between bone and muscle: the role of RANKL pathway in osteosarcopenia - 3 month(s) ago
Osteosarcopenia, which refers to the concomitant presence of osteoporosis and sarcopenia, is expected to increase in the rapidly progressive aging world, with serious clinical implications. However, the pathophysiology of osteosarcopenia has not been fully elucidated, and no optimal treatment specific to osteosarcopenia is available. The RANKL–RANK pathway is widely used as a therapeutic target for osteoporosis. Growing evidence supports the importance of the RANKL–RANK pathway, not only in bone, but also in muscle, and the therapeutic potential of targeting this pathway in muscle diseases has been noted. The muscles and bones closely communicate with each other through various secretory factors called myokines and osteokines. This review covers the roles of the RANKL–RANK pathway in the bone and muscle and their reciprocal interactions. Moreover, we will suggest future directions to move forward for the treatment of osteosarcopenia to prepare for an upcoming aging society.
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet-
Discover the first article published in our Exploring Osteoporosis and Sarcopenia special collection 💪🦶 📍 Bidirectional crosstalk between bone and muscle: the role of #RANKL pathway in #osteosarcopenia By Soo Yeon Jang and Kyung Mook Cho 👉 https://t.co/A0P5AtiQW9 https://t.co/KpXWVmFISp
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Mashup Score: 1
The root cause of type 2 diabetes (T2D) is insulin resistance (IR), defined by the failure of cells to respond to circulating insulin to maintain lipid and glucose homeostasis. While the causes of whole-body insulin resistance are multifactorial, a major contributing factor is dysregulation of liver and adipose tissue function. Adipose dysfunction, particularly adipose tissue-IR (adipo-IR), plays a crucial role in the development of hepatic insulin resistance and the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) in the context of T2D. In this review, we will focus on molecular mechanisms of hepatic insulin resistance and its association with adipose tissue function. A deeper understanding of the pathophysiological mechanisms of the transition from a healthy state to insulin resistance, impaired glucose tolerance, and T2D may enable us to prevent and intervene in the progression to T2D.
Source: joe.bioscientifica.comCategories: General Medicine News, EndocrinologyTweet-
Read this recent review by Gencer Sancar and @Dr_Birkenfeld @DiabResearch reviewing the molecular mechanisms of hepatic insulin resistance and its association with adipose tissue function ➡️ https://t.co/slFIX6QRWD https://t.co/tNaZ0ZQs99
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Read the latest article in the #Incretins Special Collection: 'Glucagon-like peptide-1 analog, liraglutide, regulates Sertoli cell energy metabolism' by Marina Ercilia Dasso et al. 👉 https://t.co/8JEe9JrKb3 #GLP1 #liraglutide #sertoli https://t.co/fSaD6XBKkF