Nanopublications

Matches in Nanopublications for { ?s ?p ?o <http://www.tkuhn.ch/bel2nanopub/RAZj8qAHkLYfMxWNfNJIwlulxjZ2zWRmiGthkDUCU-ChI#provenance>. }

Showing items 1 to 11 of 11 with 100 items per page.

_4 label "Selventa" provenance.
large_corpus.bel title "BEL Framework Large Corpus Document" provenance.
large_corpus.bel description "Approximately 61,000 statements." provenance.
large_corpus.bel version "20131211" provenance.
large_corpus.bel authoredBy _4 provenance.
assertion wasDerivedFrom large_corpus.bel provenance.
assertion wasDerivedFrom _3 provenance.
assertion hadPrimarySource 16005682 provenance.
_3 wasQuotedFrom 16005682 provenance.
_3 value "Introduction Obesity, the excessive accumulation of fat, is a risk factor for the metabolic syndrome (i.e. diabetes, dyslipidaemia and cardiovascular complications). However, not every form of obesity poses a similar clinical threat. Strong epidemiological evidence indicates that the preferential accumulation of intra-abdominal (visceral) fat, surrounding the gastrointestinal organs, poses a greater cardiovascular risk than in other forms of obesity, in which fat is preferentially accumulated under the skin (subcutaneous) in the gluteal region [1]. Confronted with the fact that the distribution of body fat might be even more relevant than the total amount of stored fat, scientists have tried, with limited success, to identify the differences between these topographically distinct depots to understand what makes the intra-abdominal depot so deleterious (Table 1). In a recent issue of Science, Fukuhara et al. [2] identified visfatin as a new protein that is preferentially produced in the intra-abdominal adipose tissue of obese mice and humans, which, surprisingly, shares many of the antidiabetic effects of insulin. This review discusses the pros and cons of visfatin action and how it might impact on future therapeutic strategies for diabetes. What is the molecular link between abdominal obesity and diabetes? An intriguing unresolved scientific question is: how does the expansion of adipose tissue, which is typically observed in obesity, result in diabetes and increased cardiovascular risk? It has been suggested that the common feature linking these problems is insulin resistance (i.e. the inability of insulin to exert its metabolic effects). In fact, obese people, in particular those who have intra-abdominal obesity, developmarked insulin resistance. Two complementary theories have been proposed to explainwhy and how obesity induces insulin resistance. One theory proposes that when adipose tissue expands excessively, it reaches a threshold level at which its storage capacity becomes saturated. As a result, it becomes less able to amass more fat. Once this stage is reached, the excess fat is redirected towards other organs, such as the liver, pancreas or muscle. In these organs, lipid accumulation can be toxic and induce insulin resistance, a phenomenon known as lipotoxicity. The second hypothesis proposes that the excessive accumulation of fat in adipose tissue can change the repertoire of adipocyte-specific secreted molecules, also known as adipokines. Interestingly, some of these adipokines modulate insulin sensitivity not only in adipose tissue but also in othermetabolically relevant organs, such as liver or muscle. This is the case for adiponectin, leptin, resistin, interleukin (IL)-6 and tumour necrosis factor (TNF)a. Therefore, the adipose tissue, in addition to being a specialized organ for fat storage, should be considered the largest endocrine gland in the body, capable of synthesizing and secreting hormones (adipokines) that can modulate insulin sensitivity locally and in other organs [3]. What is visfatin? Visfatin is a protein that is preferentially produced in visceral adipose tissue and both its tissue expression and secreted plasma levels increase in parallel with obesity. Although visfatin is preferentially produced in visceral adipose tissue, it can be found in skeletal muscle, liver, bone marrow and lymphocytes, where it was initially identified as pre-B-cell colony-enhancing factor (PBEF). Interestingly, PBEF expression is regulated by cytokines that promote insulin resistance, such as lipopolysaccharide, IL-1b, TNFa and IL-6 [4,5]." provenance.