MATERNAL LEPTIN LEVEL AS PREDICTOR MARKER IN GESTATIONAL DIABETIS MELLITUS
A.A. Fawzy (1), A.T. Tawfik (1), M.S. Swelem (1), M.M. Elberdeny (2)
1 OB/GYN Dep., School of Medicine, Alexandria, Egypt
2 Clinical Pathology Department, School of Medicine, Alexandria, Egypt
The objective of the study was to evaluate the role of Leptin as a predictor of gestational diabetes mellitus (GDM) and which precedes first: changes in leptin or abnormal glucose metabolism.
Methods: Forty pregnant ladies were selected, divided into 2 groups: G1 (study G): Twenty pregnant with GDM. G2 (Control G): Twenty normal pregnant. All were subjected to Ultrasound scan, body mass index (BMI), routine investigations, glucose challenge test (GCT), oral glucose tolerance (OGT) and measurement of serum leptin level at 16-20 and 24-28 gestational week.
Results: The leptin levels were significantly increased in G1 than G2 at different periods of gestation. The leptin levels changes happened earlier than the increase of insulin resistance. Pregnant ladies that developed GDM later had highest leptin level. Evident positive correlations were found between leptin level at 24-28 weeks and the levels of GCT OGT in G1, also, the same was observed with BMI at different periods of gestation in G1.
Conclusion: This preliminary study, confirmed that, the increased levels of leptin preceded the onset of abnormal glucose level in pregnant that developed GDM. This cytokine had a possible predictive value in GDM diagnosis. The subject is still open for further assessment, on larger number scale.
EFFECTS OF FENOFIBRATE THERAPY ON CIRCULATING ADIPOCYTOKINES IN PATIENTS WITH PRIMARY HYPERTRIGLYCERIDEMIA
K. Koh (1), M. Quon (2)
1 Gachon University Gil Hospital
2 Diabetes Unit, NIH, USA
Background: Adipocytokines including adiponectin and leptin may serve important roles in linking metabolic signals, inflammation, and atherosclerosis. We investigated effects of fenofibrate therapy on endothelial dysfunction and adipocytokine profiles.
Methods: A randomized, single-blind, placebo-controlled, cross-over study was conducted in 53 patients with primary hypertriglyceridemia. We administered placebo or fenofibrate 200 mg daily for 8 weeks.
Results: When compared with placebo, fenofibrate therapy decreased non-HDL cholesterol, apolipoprotein B, and triglycerides while increasing HDL-cholesterol and apolipoprotein A-I (all P<0.001) and decreasing total cholesterol (P<0.05). Moreover, fenofibrate therapy substantially improved the percent flow-mediated dilator response to hyperemia by 55±7% (P<0.001), lowered plasma levels of fibrinogen and TNF-a by 9±2 % (P<0.001) and 6±3 % (P=0.014), respectively, and lowered hsCRP from 1.10 to 0.90 mg/l (P=0.004). When compared with placebo, fenofibrate therapy increased plasma levels of adiponectin by 17±4% (P=0.001), insulin sensitivity by 4±1% (as assessed by QUICKI, P=0.009), and decreased plasma levels of leptin and resistin by 4±7% (P=0.022) and 10±3% (P=0.001), respectively. There were correlations between percent changes in QUICKI and percent changes in adiponectin levels (r= 0.279, P=0.043) or leptin (r= -0.280, P=0.042).
Conclusions: Fenofibrate therapy significantly improved percent flow-mediated dilator response to hyperemia, reduced pro-inflammatory biomarkers, and improved adipocytokines levels and insulin sensitivity in hypertriglyceridemic patients. Thus, actions of fenofibrate to regulate adipocytokine levels may be linked to beneficial effects on pro-inflammatory status that simultaneously improve both endothelial and metabolic function in patients with primary hypertriglyceridemia.
LEVEL OF TNF-α IN METABOLIC SYNDROME IN BANGLADESHI RURAL WOMEN
S. Mia (1,2), S. Jesmin (1,2), R. Islam (1,2), A.M.S. Islam (1,2), S.N. Sultana (1,2), S. Zaedi (1,2), N. Yamaguchi (2), M. Hiroe (2)
1 Health and Disease Research Center for Rural Peoples, Ena Arista, Baitul Aman Housing Society, Adabor, Bangladesh
2 National Center for Global Health and Medicine, Toyama, Shinjuku-ku, Tokyo, Japan
Among many inflammatory markers, tumor necrosis factor-alpha (TNF-α) emerged as a key cytokine that influences intermediary metabolism that play a great role in the development of dyslipidemia and insulin resistance as important features of the metabolic syndrome, which may eventually augment the risk of cardiovascular diseases and type 2 Diabetes Mellitus (DM). TNF-α has been demonstrated to directly interfere with the metabolic pathways of triglyceride and cholesterol. Therefore, TNF-α may gain a special importance when referring to atherosclerotic lesion development and the risk of acute cardiovascular events. The aim of the study was to observe the emergence of TNF-α level in subjects with and without Metabolic Syndrome (MS) in rural women of Bangladesh. The study subjects were recruited from the active participation of rural women of northern side in Bangladesh. Group 1 consisted of subjects without MS (non- MS) (n = 319) and group 2 consisted of subjects with MS (n = 380). MS was defined using the modified National Cholesterol Education Program Adult Treatment Panel (NCEP ATP III) criteria according to the World Health Organization Asia Pacific guidelines. The study revealed that average TNF-α level appeared as high in metabolic syndrome 8.9±0.24 (mean±SE) with compare to non metabolic syndrome (7.7±0.32, p = 0.006). It also showed that mean TNF-α increased with the increase of number of metabolic syndrome components. Body mass index (BMI) also keeping a close relation with TNF-α where mean TNF-α was increasing noticeably corresponding to increase of BMI (p=0.024).
IL-6 INDUCES MITOCHONDRIAL BIOGENESIS IN RODENT WHITE ADIPOSE TISSUE
Z. Wan (1), C. Chan (1), D. Wright (2)
1 Alberta Diabetes Institute, University of Alberta, Edmonton, Canada
2 Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Canada
Thiazolidinediones (TZDs) are a commonly prescribed class of anti-diabetic medications that appear to mediate their beneficial effects, at least in part, through the induction of adipose tissue mitochondrial biogenesis. Owing to the deleterious side effects of TZDs, the identification of alternative approaches to induce adipose tissue mitochondrial content is needed. It has been demonstrated that exercise induces adipose tissue mitochondrial biogenesis, however the hormonal factors for mediating these processes remain unidentified. Interleukin 6 (IL-6) is markedly enhanced during exercise. Thus, we hypothesized that IL-6 secreted from adipose tissue during exercise will increase mitochondrial biogenesis in white adipose tissue. An acute bout of exercise robustly increased the phosphorylation of signal transducer and activator of transcription 3 (STAT3), a signaling intermediate activated by IL-6 in adipose tissue. Similarly, exercise increased the mRNA expression of suppressor of cytokine signaling 3 (SOCS-3) in adipose tissue, a transcriptional target of IL-6. Treatment of culture adipose tissue with IL-6 (75, 150 ng/ml) for 6 hours led to approximately 2 and 3 fold increases in mRNA expression of peroxisome proliferator activated receptor co-activator 1-alpha (PGC-1α) respectively, a master regulator of mitochondrial biogenesis. To assess more directly the effects of IL-6 on adipose tissue mitochondria biogenesis, markers of mitochondrial biogenesis were measured in white adipose tissue from IL-6 knockout (IL-6-/-) mice. Citrate synthase activity and the protein content of succinate-ubiquinone oxidoreductase (SUO), cytochrome c oxidort.t.tase core I subunit (CORE1) and heat shock protein-60 (HSP60) were reduced from IL-6-/- mice. In conclusion, exercise induced adipose tissue mitochondrial biogenesis may be regulated by IL-6.