Regulation of adiponectin release and demonstration of adiponectin mRNA as well as release by the non-fat cells of human omental adipose tissue

Fain, John N.; Buehrer, Benjamin M.; Tichansky, David S.; Madan, Atul K.

doi:10.1038/sj.ijo.0803745

Cited by 30 publications

(26 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hajri et al [66] have reported that TNF-α reduced the secretion of adiponectin. A similar observation was reported by Fain et al [70]. TNF-α has also been reported to interfere with nitric oxide-mediated vasodilation [64,71,72,73].…”

Section: Infiltration Of Macrophages As a Possible Reason For The Lossupporting

confidence: 71%

Perivascular Adipose Tissue, Vascular Reactivity and Hypertension

Oriowo

2014

Med Princ Pract

View full text Add to dashboard Cite

Most blood vessels are surrounded by a variable amount of adventitial adipose tissue, perivascular adipose tissue (PVAT), which was originally thought to provide mechanical support for the vessel. It is now known that PVAT secretes a number of bioactive substances including vascular endothelial growth factor, tumor necrosis factor-alpha (TNF-α), leptin, adiponectin, insulin-like growth factor, interleukin-6, plasminogen activator substance, resistin and angiotensinogen. Several studies have shown that PVAT significantly modulated vascular smooth muscle contractions induced by a variety of agonists and electrical stimulation by releasing adipocyte-derived relaxing (ADRF) and contracting factors. The identity of ADRF is not yet known. However, several vasodilators have been suggested including adiponectin, angiotensin 1-7, hydrogen sulfide and methyl palmitate. The anticontractile effect of PVAT is mediated through the activation of potassium channels since it is abrogated by inhibiting potassium channels. Hypertension is characterized by a reduction in the size and amount of PVAT and this is associated with the attenuated anticontractile effect of PVAT in hypertension. However, since a reduction in size and amount of PVAT and the attenuated anticontractile effect of PVAT were already evident in prehypertensive rats with no evidence of impaired release of ADRF, there is the possibility that the anticontractile effect of PVAT was not directly related to an altered function of the adipocytes per se. Hypertension is characterized by low-grade inflammation and infiltration of macrophages. One of the adipokines secreted by macrophages is TNF-α. It has been shown that exogenously administered TNF-α enhanced agonist-induced contraction of a variety of vascular smooth muscle preparations and reduced endothelium-dependent relaxation. Other procontractile factors released by the PVAT include angiotensin II and superoxide. It is therefore possible that the loss could be due to an increased amount of these proinflammatory and procontractile factors. More studies are definitely required to confirm this.

show abstract

Section: Infiltration Of Macrophages As a Possible Reason For The Lossupporting

confidence: 71%

Perivascular Adipose Tissue, Vascular Reactivity and Hypertension

Oriowo

2014

Med Princ Pract

View full text Add to dashboard Cite

show abstract

“…We recognize that the adiponectin release method we used is limited to the tissue collected from the biopsy, and Bovine Serum Albumin that was used in the media may influence experimental outcome as it may contain growth factors(14). This method quantifies the amount of adiponectin released from the adipose tissue during the incubation period, which represents synthesis by adipocytes and other cells in the tissue; however, whether cells other than adipocytes contributes to circulating adiponectin in humans is still unanswered(19). …”

Section: Discussionmentioning

confidence: 99%

Addition of Exercise Increases Plasma Adiponectin and Release from Adipose Tissue

Wang

You

Murphy

et al. 2015

Medicine &Amp; Science in Sports &Amp; Exercise

View full text Add to dashboard Cite

Introduction Adiponectin is an adipose tissue-derived anti-inflammatory protein that is down-regulated in obesity. The effects of caloric restriction and exercise induced weight loss on adiponectin are not clear. Purpose To determine whether addition of aerobic exercise training to caloric restriction has additive effects over caloric restriction alone on circulating adiponectin concentrations and adiponectin release from abdominal and gluteal adipose tissue. Methods Overweight or obese (body mass index=25-40 kg/m2, waist>88 cm) postmenopausal women were randomized to 20-week caloric restriction with and without aerobic exercise (CR+EX, n=48 and CR, n=22). Blood samples were collected for measuring plasma adiponectin concentration, and abdominal and gluteal subcutaneous adipose tissue biopsies were performed in a subgroup to determine in vitro adiponectin release, before and after the interventions. Results The interventions elicited similar amounts of weight loss (CR+EX: -11.3±4.6 kg ; CR:-11.2±3.4 kg) and fat loss (CR+EX: -8.0±3.5 kg; CR:-7.4±2.7 kg). The two groups had differential changes in plasma adiponectin concentrations (p for interaction = 0.014); CR+EX increased (6.9±3.9 to 8.5±4.9 μg/ml, p= 0.0001), while CR did not alter (6.4±4.4 to 6.5±4.5 μg/ml, p=0.42), plasma adiponectin. Likewise, adiponectin release from abdominal and gluteal subcutaneous adipose tissue increased with CR+EX (p=0.0076 and 0.089, respectively), but did not change with CR (p=0.13 and 0.95, respectively). Conclusion Despite similar reductions in body weight and fat mass, the addition of aerobic exercise to caloric restriction increased plasma adiponectin concentrations, which may be partly explained by increased adiponectin release from abdominal and gluteal subcutaneous adipose tissue.

show abstract

“…Secretion of the cytokine TNFα in adipose tissue alters the differentiation of preadipocytes, and reduces adiponectin secretion (Fain, et al, 2008). TNFα is a pleiotropic cytokine that can exert a variety of effects including growth promotion and inhibition, cytotoxicity, and inflammation (Balkwill, 2009).…”

Section: Introductionmentioning

confidence: 99%

TallyHO obese female mice experience poor reproductive outcomes and abnormal blastocyst metabolism that is reversed by metformin

Louden

Luzzo

Jimenez

et al. 2015

Reprod. Fertil. Dev.

View full text Add to dashboard Cite

Objective Obese women experience worse reproductive outcomes compared to normal weight women, specifically infertility, pregnancy loss, fetal malformations and developmental delay. The objective of this study was to use a genetic mouse model of obesity in order to recapitulate the human reproductive phenotype and further examine potential mechanisms and therapies. Methods New inbred, polygenic Type 2 diabetic TallyHO mice and age matched control C57BL/6 mice were superovulated to obtain morulae or blastocysts stage embryos which were cultured in human tubal fluid media. Deoxyglucose uptake was performed on insulin-stimulated individual blastocysts. Apoptosis was detected by confocal microscopy using TUNEL assay and Topro-3 nuclear dye. Embryos were scored for %TUNEL positive/total nuclei. AMPK activation, TNFα expression, and adiponectin expression were analyzed by western immunoblot and confocal immunofluorescent microscopy. Lipid accumulation was assayed by Bodipy. Finally all measured parameters were compared between TallyHO mice in morulaes cultured to blastocyst embryos in either human tubal fluid (HTF) media or HTF with 25ug/ml metformin added. Results TallyHo mice developed whole body abnormal insulin tolerance, decreased litter number and increased NEFA. Blastocysts demonstrated increased apoptosis, decreased insulin sensitivity, and decreased activation of AMP activated protein-kinase (AMPK). As a possible cause of the insulin resistance/abnormal P-AMPK, we found that Tumor necrosis Factor (TNFα) expression and lipid accumulation as detected by BODIPY were increased in TallyHO blastocysts and adiponectin was decreased. Culturing TallyHO morulae with the AMPK activator, metformin lead to a reversal of all abnormal findings, including increased p-AMPK, improved insulin-stimulated glucose uptake and normalization of lipid accumulation. Conclusions Women with obesity and insulin resistance experience poor pregnancy outcomes. Previously we have shown in mouse models of insulin resistance that AMPK activity is decreased and that activators of AMPK reverse the poor embryo outcomes. Here, we show for the first time using a genetically altered obese model, not a diet-induced model, that metformin reverses many of the adverse effects of obesity at the level of the blastocyst. Expanding on this we determine that activation of AMPK via metformin reduces lipid droplet accumulation, presumably by eliminating the inhibitory effects of TNFα, resulting in normalization of fatty acid oxidation and HADH2 activity. Metformin exposure in vitro was able to partially reversing these effects, at the level of the blastocyst and thus may be effective in preventing the adverse effects of obesity on pregnancy and reproductive outcomes.

show abstract

Regulation of adiponectin release and demonstration of adiponectin mRNA as well as release by the non-fat cells of human omental adipose tissue

Cited by 30 publications

References 38 publications

Perivascular Adipose Tissue, Vascular Reactivity and Hypertension

Perivascular Adipose Tissue, Vascular Reactivity and Hypertension

Addition of Exercise Increases Plasma Adiponectin and Release from Adipose Tissue

TallyHO obese female mice experience poor reproductive outcomes and abnormal blastocyst metabolism that is reversed by metformin

Contact Info

Product

Resources

About