SwePub
Sök i SwePub databas

  Extended search

Träfflista för sökning "L773:1879 3061 OR L773:1043 2760 srt2:(2020-2024)"

Search: L773:1879 3061 OR L773:1043 2760 > (2020-2024)

  • Result 1-10 of 22
Sort/group result
   
EnumerationReferenceCoverFind
1.
  •  
2.
  • Alexandraki, Krystallenia I., et al. (author)
  • Endocrinological Toxicity Secondary to Treatment of Gastroenteropancreatic Neuroendocrine Neoplasms (GEP-NENs)
  • 2020
  • In: Trends in endocrinology and metabolism. - : Elsevier. - 1043-2760 .- 1879-3061. ; 31:3, s. 239-255
  • Journal article (peer-reviewed)abstract
    • Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) are increasingly recognized, characterized by prolonged survival even with metastatic disease. Their medical treatment is complex involving various specialties, necessitating awareness of treatment-related adverse effects (AEs). As GEP-NENs express somatostatin receptors (SSTRs), long-acting somatostatin analogs (SSAs) that are used for secretory syndrome and tumor control may lead to altered glucose metabolism. Everolimus and sunitinib are molecular targeted agents that affect glucose and lipid metabolism and may induce hypothyroidism or hypocalcemia, respectively. Chemotherapeutic drugs can affect the reproductive system and water homeostasis, whereas immunotherapeutic agents can cause hypophysitis and thyroiditis or other immune-mediated disorders. Treatment with radiopeptides may temporarily lead to radiation-induced hormone disturbances. As drugs targeting GEP-NENs are increasingly introduced, recognition and management of endocrine-related AEs may improve compliance and the quality of life of these patients.
  •  
3.
  • Balgoma, David, et al. (author)
  • Etherglycerophospholipids and ferroptosis : structure, regulation, and location
  • 2021
  • In: Trends in endocrinology and metabolism. - : Elsevier. - 1043-2760 .- 1879-3061. ; 32:12, s. 960-962
  • Journal article (other academic/artistic)abstract
    • Two pioneering studies by Zou et al. and Cui et al. have reported that the synthesis of etherglycerophospholipids (etherPLs) sensitizes cells to ferroptosis. The location and regulation of etherPLs suggest that: (i) lipid peroxidation in the inner leaflet of the plasma membrane might be of importance in ferroptosis, and (ii) different etherPLs may differently sensitize cells to ferroptosis.
  •  
4.
  •  
5.
  • Cannon, Barbara, et al. (author)
  • A PERKy way to make mitochondrial cristae
  • 2021
  • In: Trends in endocrinology and metabolism. - : Elsevier BV. - 1043-2760 .- 1879-3061. ; 32:7, s. 417-419
  • Research review (peer-reviewed)abstract
    • PERK protein, that is canonically associated with the response to endoplasmic reticulum stress, may be acquiring a new role as a regulator of the growth of mitochondrial cristae. This role is pertinent not only to the recruitment of brown adipose tissue thermogenic capacity but probably also to directing cristae formation in highly metabolically active organs such as the heart.
  •  
6.
  •  
7.
  • Gurzov, Esteban N., et al. (author)
  • Novel Strategies to Protect and Visualize Pancreatic beta Cells in Diabetes
  • 2020
  • In: Trends in endocrinology and metabolism. - : Elsevier. - 1043-2760 .- 1879-3061. ; 31:12, s. 905-917
  • Research review (peer-reviewed)abstract
    • A common feature in the pathophysiology of different types of diabetes is the reduction of beta cell mass and/or impairment of beta cell function. Diagnosis and treatment of type 1 and type 2 diabetes is currently hampered by a lack of reliable techniques to restore beta cell survival, to improve insulin secretion, and to quantify beta cell mass in patients. Current new approaches may allow us to precisely and specifically visualize beta cells in vivo and provide viable therapeutic strategies to preserve, recover, and regenerate beta cells. In this review, we discuss recent protective approaches for beta cells and the advantages and limitations of current imaging probes in the field.
  •  
8.
  • Haikonen, Retu, et al. (author)
  • Diet- and microbiota-related metabolite, 5-aminovaleric acid betaine (5-AVAB), in health and disease
  • 2022
  • In: Trends in Endocrinology and Metabolism. - : Elsevier BV. - 1879-3061 .- 1043-2760. ; 33:7, s. 463-480
  • Research review (peer-reviewed)abstract
    • 5-Aminovaleric acid betaine (5-AVAB) is a trimethylated compound associated with the gut microbiota, potentially produced endogenously, and related to the dietary intake of certain foods such as whole grains. 5-AVAB accumulates within the metabolically active tissues and has been typically found in higher concentrations in the heart, muscle, and brown adipose tissue. Furthermore, 5-AVAB has been associated with positive health effects such as fetal brain development, insulin secretion, and reduced cancer risk. However, it also has been linked with some negative health outcomes such as cardiovascular disease and fatty liver disease. At the cellular level, 5-AVAB can influence cellular energy metabolism by reducing β-oxidation of fatty acids. This review will focus on the metabolic role of 5-AVAB with respect to both physiology and pathology. Moreover, the analytics and origin of 5-AVAB and related compounds will be reviewed.
  •  
9.
  • Keipert, Susanne, et al. (author)
  • Stress-induced FGF21 and GDF15 in obesity and obesity resistance
  • 2021
  • In: Trends in endocrinology and metabolism. - : Elsevier BV. - 1043-2760 .- 1879-3061. ; 32:11, s. 904-915
  • Research review (peer-reviewed)abstract
    • Fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15) are established as stress-responsive cytokines that can modulate energy balance by increasing energy expenditure or suppressing food intake, respectively. Despite their pharmacologically induced beneficial effects on obesity and comorbidities, circulating levels of both cytokines are elevated during obesity and related metabolic complications. On the other hand, endocrine crosstalk via FGF21 and GDF15 was also reported to play a crucial role in genetically modified mouse models of mitochondrial perturbations leading to diet-induced obesity (DIO) resistance. This review aims to dissect the complexities of endogenous FGF21 and GDF15 action in obesity versus DIO resistance for the regulation of energy balance in metabolic health and disease.
  •  
10.
  •  
Skapa referenser, mejla, bekava och länka
  • Result 1-10 of 22
Type of publication
journal article (15)
research review (7)
Type of content
peer-reviewed (20)
other academic/artistic (2)
Author/Editor
Kroemer, G (2)
Tobias, J. (1)
Falhammar, H (1)
Sharma, N. (1)
Zhou, H. (1)
Vosough, M (1)
show more...
Bulik, CM (1)
Carroll, IM (1)
Duran, I (1)
Calissendorff, J (1)
Cannon, Barbara (1)
Nedergaard, Jan (1)
Furlan, A (1)
Mellgren, G (1)
Lip, GYH (1)
Ragnarsson, Oskar, 1 ... (1)
Ahlgren, Ulf (1)
Gotthardt, Martin (1)
Mäkitie, O (1)
Koistinen, Ville Mik ... (1)
Kärkkäinen, Olli (1)
Hanhineva, Kati, 197 ... (1)
Rivadeneira, F (1)
Kopietz, Franziska (1)
Göransson, Olga (1)
Gustafsson, JA (1)
Najimi, M (1)
Ajoolabady, A (1)
Wang, SY (1)
Aslkhodapasandhokmab ... (1)
Ren, J (1)
Libby, P (1)
Tuomeilehto, J (1)
Penninger, JM (1)
Richarrdson, DR (1)
Tang, DL (1)
Kionsky, DJ (1)
Hedeland, Mikael (1)
Daskalakis, Kosmas, ... (1)
Ferno, J (1)
Bjorkstrom, NK (1)
Aleksejeva, E (1)
Salumets, A (1)
Esteki, MZ (1)
Tsoli, Marina (1)
Alexandraki, Krystal ... (1)
Kaltsas, Gregory A. (1)
Grossman, Ashley B. (1)
Brandi, ML (1)
Gabet, Y. (1)
show less...
University
Karolinska Institutet (14)
University of Gothenburg (2)
Stockholm University (2)
Umeå University (1)
Uppsala University (1)
Örebro University (1)
show more...
Lund University (1)
Chalmers University of Technology (1)
The Swedish School of Sport and Health Sciences (1)
show less...
Language
English (22)
Research subject (UKÄ/SCB)
Medical and Health Sciences (10)
Natural sciences (1)

Year

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Close

Copy and save the link in order to return to this view