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JournalISSN: 1043-2760

Trends in Endocrinology and Metabolism 

Elsevier BV
About: Trends in Endocrinology and Metabolism is an academic journal published by Elsevier BV. The journal publishes majorly in the area(s): Receptor & Insulin resistance. It has an ISSN identifier of 1043-2760. Over the lifetime, 2646 publications have been published receiving 195779 citations. The journal is also known as: TEM & Trends in endocrinology & metabolism.


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Journal ArticleDOI
TL;DR: The discovery of leptin in the mid-1990s has focused attention on the role of proteins secreted by adipose tissue, which is also involved in the regulation of neuroendocrine and immune function and the metabolic and cardiovascular complications associated with obesity.
Abstract: Adipose tissue is a complex, essential, and highly active metabolic and endocrine organ. Besides adipocytes, adipose tissue contains connective tissue matrix, nerve tissue, stromovascular cells, and immune cells. Together these components function as an integrated unit. Adipose tissue not only responds to afferent signals from traditional hormone systems and the central nervous system but also expresses and secretes factors with important endocrine functions. These factors include leptin, other cytokines, adiponectin, complement components, plasminogen activator inhibitor-1, proteins of the renin-angiotensin system, and resistin. Adipose tissue is also a major site for metabolism of sex steroids and glucocorticoids. The important endocrine function of adipose tissue is emphasized by the adverse metabolic consequences of both adipose tissue excess and deficiency. A better understanding of the endocrine function of adipose tissue will likely lead to more rational therapy for these increasingly prevalent disorders. This review presents an overview of the endocrine functions of adipose tissue. (J Clin Endocrinol Metab 89: 2548–2556, 2004)

1,513 citations

Journal ArticleDOI
TL;DR: A strong correlation between plasma Acrp30 levels and systemic insulin sensitivity is well established and the protein has putative anti-atherogenic properties that are relevant for the prevention of formation of atherosclerotic plaques.
Abstract: In recent years, we have learned that adipocytes are not merely inert storage depots for triglycerides but rather highly active cells with potent autocrine, paracrine and endocrine functions. Adipose tissue secretes a large number of physiologically active polypeptides. Although leptin remains one of the best-studied examples of an adipocyte-specific secretory factor, recent reports describe potent physiological activities for another adipocyte-specific secreted protein, adipocyte complement-related protein of 30 kDa (Acrp30). Full-length versions of Acrp30 or its proteolytic fragments decrease the postprandial rise of plasma free fatty acids and improve postabsorptive insulin-mediated suppression of hepatic glucose output. A strong correlation between plasma Acrp30 levels and systemic insulin sensitivity is well established and the protein has putative anti-atherogenic properties that are relevant for the prevention of formation of atherosclerotic plaques. The current challenge is to understand the molecular mechanisms through which the protein exerts its multiple functions.

1,199 citations

Journal ArticleDOI
TL;DR: The ways in which metabolic alterations convey changes in mitochondrial morphology and how disruption of mitochondrial morphology impacts cellular and organismal metabolism are reviewed.
Abstract: Mitochondrial morphology varies tremendously across cell types and tissues, changing rapidly in response to external insults and metabolic cues, such as nutrient status. The many functions of mitochondria have been intimately linked to their morphology, which is shaped by ongoing events of fusion and fission of outer and inner membranes (OM and IM). Unopposed fission causes mitochondrial fragmentation, which is generally associated with metabolic dysfunction and disease. Unopposed fusion results in a hyperfused network and serves to counteract metabolic insults, preserve cellular integrity, and protect against autophagy. Here, we review the ways in which metabolic alterations convey changes in mitochondrial morphology and how disruption of mitochondrial morphology impacts cellular and organismal metabolism.

854 citations

Journal ArticleDOI
TL;DR: Results reveal previously unsuspected roles for 1,25-(OH)(2)D(3) in brain function and suggest possible areas of future research, including neuroprotective and immunomodulatory effects in neurodegenerative and neuroimmune diseases.
Abstract: Accumulating data have provided evidence that 1 alpha,25 dihydroxyvitamin D(3) [1,25-(OH)(2)D(3)] is involved in brain function. Thus, the nuclear receptor for 1,25-(OH)(2)D(3) has been localized in neurons and glial cells. Genes encoding the enzymes involved in the metabolism of this hormone are also expressed in brain cells. The reported biological effects of 1,25-(OH)(2)D(3) in the nervous system include the biosynthesis of neurotrophic factors and at least one enzyme involved in neurotransmitter synthesis. 1,25-(OH)(2)D(3) can also inhibit the synthesis of inducible nitric oxide synthase and increase glutathione levels, suggesting a role for the hormone in brain detoxification pathways. Neuroprotective and immunomodulatory effects of this hormone have been described in several experimental models, indicating the potential value of 1,25-(OH)(2)D(3) pharmacological analogs in neurodegenerative and neuroimmune diseases. In addition, 1,25-(OH)(2)D(3) induces glioma cell death, making the hormone of potential interest in the management of brain tumors. These results reveal previously unsuspected roles for 1,25-(OH)(2)D(3) in brain function and suggest possible areas of future research.

818 citations

Journal ArticleDOI
TL;DR: Evidence indicates that acute, subacute or chronic stress might suppress cellular immunity but boost humoral immunity, mediated by a differential effect of stress hormones, the glucocorticoids and catecholamines, on T helper 1 (Th1)/Th2 cells and type 1/type 2 cytokine production.
Abstract: In general, stress has been regarded as immunosuppressive. Recent evidence, however, indicates that acute, subacute or chronic stress might suppress cellular immunity but boost humoral immunity. This is mediated by a differential effect of stress hormones, the glucocorticoids and catecholamines, on T helper 1 (Th1)/Th2 cells and type 1/type 2 cytokine production. Furthermore, acute stress might induce pro-inflammatory activities in certain tissues through neural activation of the peripheral corticotropin-releasing hormone-mast cell-histamine axis. Through the above mechanisms, stress might influence the onset and/or course of infectious, autoimmune/inflammatory, allergic and neoplastic diseases.

778 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202359
202295
2021106
202093
201996
201898