Elevated Plasma Level of Visfatin/Pre-B Cell Colony-Enhancing Factor in Patients with Type 2 Diabetes Mellitus

Chen, Miao-Pei; Chung, Fu‐Mei; Chang, De-Kuan; Tsai, Jack C.-R.; Huang, Han-Fen; Shin, Shyi–Jang; Lee, Yau-Jiunn

doi:10.1210/jc.2005-1475

Cited by 596 publications

(543 citation statements)

References 34 publications

Supporting

Mentioning

469

Contrasting

Unclassified

Order By: Relevance

“…Thus, in addition to its relationship with visceral fat, visfatin quantification may also serve as a marker of glucose homeostasis. This is supported by reports demonstrating that visfatin expression and release is increased in obese subjects and in patients with type 2 diabetes mellitus [7,8] where plasma concentrations are substantially higher than in healthy young subjects. Plasma visfatin concentrations using this assay are generally <1.0 ng/ml in healthy young subjects.…”

Section: Discussionsupporting

confidence: 68%

“…Circulating visfatin concentrations were found to be correlated with the amount of visceral fat in healthy non-obese humans [6], consistent with the finding that increased visfatin release and expression is associated with obesity and diabetes in this tissue [7,8]. Further, increased plasma visfatin concentrations were reduced after weight loss in morbidly obese subjects [9].…”

supporting

confidence: 77%

See 1 more Smart Citation

The release of the adipocytokine visfatin is regulated by glucose and insulin

et al. 2006

View full text Add to dashboard Cite

Aims/hypothesis The novel insulin-mimetic adipocytokine visfatin has been linked to the metabolic syndrome, but its regulation has not been characterised to date. Since insulinmimetic actions of visfatin may be part of the feedback regulation of glucose homeostasis, we hypothesised that visfatin concentrations are influenced by glucose or insulin blood levels in humans. Subjects, materials and methods In this randomised, doubleblind, placebo-controlled crossover study, nine healthy male subjects (age 26±6 years) attended three different study days. On each day, systemic glucose concentrations of 5.0, 8.3 and 11.1 mmol/l were attained by stepwise increases in i.v. infusions of glucose, representing fasting and postprandial conditions. Visfatin plasma concentrations were studied during concomitant exogenous hyperinsulinaemia, inhibition of endogenous insulin production by somatostatin infusion, and placebo time control. Additionally, human adipocytes were cultured to study visfatin release and mRNA expression in vitro.Results Glucose concentrations of 8.3 and 11.1 mmol/l increased circulating visfatin from baseline concentrations of 0.5±0.0 ng/ml to 0.9±0.1 and 2.1±0.3 ng/ml, respectively (p<0.01). Glucose-induced elevation of visfatin was prevented by co-infusion of insulin or somatostatin (p<0.05). Cultured subcutaneous and visceral adipocytes released an equivalent amount of visfatin upon glucose-concentrationand time-dependent stimulation. Visfatin secretion involved the phosphatidylinositol 3-kinase (PI3-kinase) and protein kinase B (AKT) pathways. The mRNA expression pattern of visfatin was consistent with this altered protein release. Conclusions/interpretation Circulating visfatin concentrations are increased by hyperglycaemia. This effect is suppressed by exogenous hyperinsulinaemia or somatostatin infusion. Glucose signalling for visfatin release in adipocytes involves the PI3-kinase/AKT pathway.

show abstract

Section: Discussionsupporting

confidence: 68%

supporting

confidence: 77%

The release of the adipocytokine visfatin is regulated by glucose and insulin

et al. 2006

View full text Add to dashboard Cite

show abstract

“…In humans, the normal fasting PBEF level is 10-40 ng/ml [1][2][3][4][5], which equals 180-700 pmol/l for this 55 kDa protein, 3.6-14 times the concentration of the normal fasting insulin level (50 pmol/l). If PBEF could act with the same efficacy as insulin [1], it should contribute importantly to the regulation of glucose metabolism.…”

Section: Discussionmentioning

confidence: 93%

“…Visfatin was also shown to mimic the effect of insulin with the same efficacy in rodent cells in vitro and in mouse models [1]. However, subsequent studies in human subjects reported conflicting results with regard to its relation with adiposity [2][3][4], subcutaneous or visceral fat [2,3], and insulin resistance [3][4][5], suggesting that the role of this protein in the development of obesity and insulin resistance remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“…In this case, familial combined hyperlipidemia (FCHL) family relatives were chosen because FCHL is a disorder of lipoprotein metabolism in the presence of insulin resistance, and it is known that the accumulation of abdominal fat, especially visceral fat, is highly prevalent in FCHL families [11]. To avoid the influence of type 2 diabetes [4,5], only non-diabetic subjects were enrolled in this study.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The circulating PBEF/NAMPT/visfatin level is associated with a beneficial blood lipid profile

Wang

Greevenbroek

Bouwman

et al. 2007

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

Visfatin with the official gene name pre-B cell colony-enhancing factor 1 (PBEF) and the protein name nicotinamide phosphoribosyltransferase (NAMPT) is a recently discovered adipocyte-secreted protein that was shown by some to be associated with visceral fat and insulin resistance. To explore the link between PBEF/ NAMPT/visfatin and lipid metabolism, we analyzed the relation of its plasma level with several parameters of adiposity, insulin resistance and the circulating blood lipid profile in a group of general population (n=40) and a group of subjects who are genetically predisposed to insulin resistance and hyperlipidemia (n=35). In both groups and pooled cohort, PBEF/NAMPT/visfatin lacked association with whole body adiposity, but correlated positively with HDL-cholesterol and negatively with triglycerides. The data suggested a negative correlation of the PBEF level with visceral fat and insulin resistance. But this negative correlation completely disappeared after adjustment for lipid profile. We concluded that circulating PBEF/NAMPT/ visfatin level is an indicator of beneficial lipid profile in non-diabetic Caucasian subjects. The relation to lipid metabolism does not depend on visceral obesity and insulin resistance, but may be linked to its enzymatic function in NAD metabolism.

show abstract

Roles of Gastrointestinal and Adipose Tissue Peptides in Childhood Obesity and Changes After Weight Loss Due to Lifestyle Intervention

Roth

Reinehr

2010

Arch Pediatr Adolesc Med

View full text Add to dashboard Cite

hildhood obesity is a global epidemic and associated with an increased risk of hypertension, diabetes mellitus, and coronary heart disease, in addition to psychological disorders. Interventions such as bariatric surgery are highly invasive and lifestyle modifications are often unsuccessful because of disturbed perceptions of satiety. New signaling peptides discovered in recent years that are produced in peripheral tissues such as the gut, adipose tissue, and pancreas communicate with brain centers of energy homeostasis, such as the hypothalamus and hindbrain. This review discusses the major known gut-and adipose tissuederived hormones involved in the regulation of food intake and energy homeostasis and their serum levels in childhood obesity before and after weight loss as well as their relationship to consequences of obesity. Since most of the changes of gastrointestinal hormones and adipokines normalize in weight loss, pharmacological interventions based on these hormones will likely not solve the obesity epidemic in childhood. However, a better understanding of the pathways of body weightand food intake-regulating gut-and adipose tissue-derived hormones will help to find new strategies to treat obesity and its consequences.

show abstract

Elevated Plasma Level of Visfatin/Pre-B Cell Colony-Enhancing Factor in Patients with Type 2 Diabetes Mellitus

Abstract: Our results indicate that visfatin may play a role in the pathogenesis of T2DM.

Cited by 596 publications

References 34 publications

The release of the adipocytokine visfatin is regulated by glucose and insulin

The release of the adipocytokine visfatin is regulated by glucose and insulin

The circulating PBEF/NAMPT/visfatin level is associated with a beneficial blood lipid profile

Roles of Gastrointestinal and Adipose Tissue Peptides in Childhood Obesity and Changes After Weight Loss Due to Lifestyle Intervention

Contact Info

Product

Resources

About