Adiponectin and inflammation: Consensus and controversy
Circulating levels of adiponectin decrease with increasing visceral obesity and are lower in patients with type 2 diabetes, the metabolic syndrome, and cardiovascular disease compared with controls matched by body mass index. Several reports demonstrated anti-inflammatory effects of adiponectin. Because increased adipose tissue is associated with low-grade chronic inflammation and proinflammatory factors inhibit adiponectin production, the current hypothesis states that chronic inflammation associated with visceral obesity inhibits production of adiponectin, perpetuating inflammation. The negative correlation between adiponectin and markers of inflammation in the aforementioned conditions supports this hypothesis. In contrast with disorders typically associated with excess adiposity and positive energy balance, adiponectin levels are elevated--rather than decreased--in classic chronic inflammatory/autoimmune diseases that are unrelated to increased adipose tissue, such as rheumatoid arthritis, SLE, inflammatory bowel disease, type 1 diabetes, and cystic fibrosis. In these patients, adiponectin levels positively--rather than negatively--correlate with inflammatory markers. Furthermore, proinflammatory effects of adiponectin have been reported in tissues such as joint synovium and colonic epithelium. Thus, adiponectin is regulated in the opposite direction and may exert differential functions in classic versus obesity-associated inflammatory conditions. This article discusses this apparent paradox and presents possible alternative and/or complementary explanations.
Available from: Emre Sarandol
- "The levels of adiponectin, which is regarded as an antidiabetic, antiinflammatory , and antiatherogenic cytokine, are reported to be depressed in patients with type 2 DM  . However, in some studies, increased adiponectin levels have been reported in patients with type 1 DM . Resistin, on the other hand, impairs cellular glucose intake, because it is stimulated by insulin; as a result, hepatic glucose production is increased, leading to impaired glucose tolerance and eventual development of insulin resistance. "
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ABSTRACT: Aim. To investigate the efficacy of combined therapy of insulin and rosiglitazone on metabolic and inflammatory parameters, insulin sensitivity, and adipocytokine levels in patients with type 1 diabetes mellitus (type 1 DM). Material and Methods. A total of 61 adults with type 1 DM were randomly and prospectively assigned in open-label fashion to take insulin and rosiglitazone 4 mg/day (n = 30) or insulin alone (n = 31) for a period of 18 weeks while undergoing insulin therapy without acute metabolic complications. Results. Combination therapy did not significantly improve metabolic and inflammatory parameters, insulin sensitivity, and adiponectin levels. While leptin and resistin levels decreased in both groups (group 1: resistin 6.96 ± 3.06 to 4.99 ± 2.64, P = 0.006; leptin 25.8 ± 17.6 to 20.1 ± 12.55, P = 0.006; group 2: resistin 7.16 ± 2.30 to 5.57 ± 2.48, P = 0.031; leptin 16.72 ± 16.1 to 14.0 ± 13.4, P = 0.007) Hgb and fibrinogen levels decreased only in group 1 (Hgb 13.72 ± 1.98 to 13.16 ± 1.98, P = 0.015, and fibrinogen 4.00 ± 1.08 to 3.46 ± 0.90, P = 0.002). Patients in both groups showed weight gain and the incidence of hypoglycemia was not lower. Discussion. The diverse favorable effects of TZDs were not fully experienced in patients with type 1 DM. These results are suggesting that insulin sensitizing and anti-inflammatory characteristics of TZDs were likely to be more pronounced in patients who were not totally devoid of endogenous insulin secretion.
Available from: Vincenzo Vincenti
- "This was also our experience in the patient who underwent re-implantation. We usually utilise abdominal fat because of its easy availability, low metabolic rate and resistance to necrosis; in addition, fat has been reported to have intrinsic immunoreactive features that may overcome infection 20. Regarding the problem of radiological assessment, undoubtedly the presence of fat makes interpretation of HRCT scans more difficult, but detection of soft tissue expansion or temporal bone erosion revealing the development of cholesteatoma is possible. "
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ABSTRACT: COCHLEAR IMPLANTATION IN THE SETTING OF CHRONIC OTITIS MEDIA OR PREVIOUS MIDDLE EAR SURGERY POSES SEVERAL PROBLEMS FOR THE SURGEON: possible spread of infection to the cochlea and the subarachnoid spaces with consequent meningitis, risk of electrode array extrusion and possible recurrence of the original disease. Several surgical strategies have been proposed to overcome these problems. In the present study, clinical and functional results of cochlear implantation in 26 patients with chronic otitis media (8 cases) or previous middle ear surgery (18 cases) in the ear most suitable for implantation were retrospectively reviewed. Among the 8 patients with chronic otitis media, in 7 cases a subtotal petrosectomy associated with external auditory canal closure and mastoid and Eustachian tube obliteration was performed, while in the remaining patient cochlear implantation was done 6 months after a myringoplasty. The only complication observed was a reperforation of the tympanic membrane in this latter patient. Among the 18 patients with previous middle ear surgery, 2 had undergone intact canal wall tympanomastoidectomy and were implanted utilising the previous surgical approach. In the remaining 16 patients who had a radical cavity, an open technique was maintained in 3 cases; a cavity revision associated to external auditory canal closure, Eustachian tube and mastoid obliteration was performed in 12 patients, while in one case a middle cranial fossa approach was utilised. Two of the 3 patients in whom an open technique was maintained have experienced electrode array extrusion. The only complication observed in the remaining patients was the breakdown of the external auditory canal closure in one case. No problems were noted in patients who had undergone intact canal wall tympanomastoidectomy as well as in the subject implanted via the middle cranial fossa approach. All patients achieved and maintained good hearing performance over time. Subtotal petrosectomy associated with external auditory canal closure, Eustachian tube occlusion and mastoid obliteration is an effective procedure to facilitate cochlear implantation in presence of chronic otitis media. The open cavity technique offers the advantage of a close clinical examination, but may expose the patient to the risk of electrode array extrusion, mainly in the long-term period.
Available from: Sophia E Schiza
- ". Moreover, in vitro studies demonstrate that the above inflammatory factors suppress the production of adiponectin, which is released from adipose cells and exerts a variety of anti-inflammatory effects . The underlying mechanisms by which OSAHS and ED interact are still unknown. "
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ABSTRACT: Patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) show a high prevalence of erectile dysfunction (ED). Although the underlying pathogenesis is still unknown, endothelial dysfunction, induced by inflammatory cytokines, chemokines, and adhesion molecules, has been proposed as a possible mechanism. The aim of this study was to assess whether OSAHS is associated with activation of the inflammatory cytokine system in patients with ED compared to the matched OSAHS patients with normal sexual function. Thirty-one patients with severe OSAHS and ED were included. Fifteen patients with severe OSAHS and without ED served as controls. Serum concentrations of high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor- α (TNF-a), interleukin-6 (IL-6), interleukin-8 (IL-8), and adiponectin were measured after the diagnostic polysomnography. We found that hsCRP levels were significantly elevated in OSAHS patients with ED compared to controls. Similarly, TNF-a levels, IL-6, and IL-8 were elevated in OSAHS patients with ED compared to controls. Serum adiponectin levels were lower in OSAHS-ED patients, but the difference did not reach statistical significance. The presence of ED in patients with severe OSAHS is associated with elevated levels of inflammatory markers, underlining a possible involvement of endothelial dysfunction in the pathogenesis of ED.
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