Academic literature on the topic 'Insulin sensivity'

BACKGROUND: Obesity is highly related to insulin resistance, therefore, the increased number of obesity is followed by the increased prevalence of type 2 Diabetes Melitus. Obesity is associated with increased of reactive oxygen species (ROS) in muscle, liver and endothelial cells. The increase of ROS would lead to insulin resistance (IR) and increased proinflamatory protein. FFA plays an important role in IR by inhibiting muscle glucose transport and oxidation via effects on serin/threonine phosphorylation of IRS-1. The aim of this study was discover the existence of SOD, hs-CRP and and adiponectin levels towards the occurrence of insulin resistance which was caused by elevated level of FFA and to discover the interaction between SOD, hs-CRP and adiponectin in non diabetic obese adult male.METHOD: This was observational study with cross sectional design. There were 65 obese male non diabetic subjects and 45 non obese male non diabetic subjects who met the criteria. In this study, measurements were done on body mass index (BMI), fasting glucose, insulin, adiponectin, hs-CRP and SOD. Obese was defined as BMI >25 kg/m2, normal weight was defined as BMI 18.5-23 kh/m2 and Insulin Resistance was defined as HOMA-IR >1.RESULT: This study showed that Hypoadiponectinemia condition, decreased SOD level and high level of hs-CRP is associated with insulin resistance in obese non diabetic subject. Adiponectin and SOD were correlated negatively with insulin resistance in obese non diabetic (Adiponectin, r=-0.455, p<0.001; SOD, r=-0.262, p=0.003), hs-CRP was positively correlated with insulin resistance in obese non diabetic (r=0.592, p<0.001). FFA levels was increased in obese insulin resistance compared with non obese non insulin resistance. The Odds Ratio of Adiponectin, hs-CRP and SOD in this study was analyzed by logistic binary. The OR for SOD 3.6 (p=0.001), hs-CRP 9.1 (p<0.001) and Adiponectin 7.2 (p<0.001).CONCLUSION: This study suggested that FFA levels increased in obese insulin resistance as compared with non obese non insulin resistance. Hypoadiponectinemia, decreased SOD and elevated hs-CRP were associated with insulin resistance in obese non diabetic subjects.KEYWORDS: obesity, insulin resistance, FFA, SOD, hs-CRP, adiponectin

Efektifitas Strecting dan Electrical Stimulation pada Penderita Diabetes Mellitus Tipe 2 Dewy Haryanti1, Rika Wahyuni Arsianti2, Hendy Lesmana3Dosen Universitas Borneo Tarakan ABSTRAK artikel ini membahas tentang keefektifan Strecting dengan Electrical Stimulation pada otot pasien Diabetes melitus Tipe 2 . pilar penanganan diabetes melitus ada 4 yaitu, edukasi, diet, latihan fisik dan obat obatan. Latihan fisik sangat penting pada pasien diabetes melitus, namun tidak semua penderita diabetes mellitus mampu melakukan latihan fisik secara maksimal seperti jogging atau senam aerobic yang membutuhkan kekuatan yang lebih besar dalam pelaksanaannya. faktor usia dan lain-lain menjadi penyebab utama dalam keterbatasan melakukan aktifitas fisik. Salah satu alternatif melakukan latihan fsik adalah strecting ( Dewy, 2014) untuk mengontrol nilai glukosa darah. Strecting merupakan suatu alternatif dalam melakukan latihan fisik, begitupun dengan Electrical Stimulation pada otot pasien diabetes Melitus. Penelitian ini bertujuan untuk melihat keefktifan strecting dengan Electricla stimulation pada Otot yang berkontraksi dapat meningkatkan sensivitas insulin sehingga dapat menurunkan kadar glukosa dalam darah. Melalui analisa statistik Uji- T terhadap data hasil penelitian diperoleh bahwa Strecting dan pemberian Electrical Stimulation keduanya efektif menurunkan nilai glukosa darah pada pasien diabetes melitus tipe 2. Hanya sj dilihat dari nilai statistic maka strecting memiliki kemampuan lebih baik dari Electrical Stimulation dalam menurunkan nilai glukosa darah. Kata Kunci— Strecting, Electrical Stimulation, Latihan Fisik, Glukosa Darah, Diabetes Mellitus Tipe 2.

Intrauterine growth restriction (IUGR) and neonatal catch-up growth are risk factors for the development of metabolic disease in later life. Developmental programming of insulin resistance is hypothesised to underpin many of these disorders. Animal models are required to investigate the mechanisms underlying this programming of insulin resistance and metabolic disease. Therefore, the current study assessed the effects of spontaneous growth restriction due to natural variation in litter size in the guinea pig on programming of adult metabolic outcomes. Increasing litter size reduced birth weight, birth length and birth weight to length ratio while head dimensions at birth were relatively conserved, indicating head sparing and asymmetrical IUGR. Offspring from larger litters displayed faster neonatal fractional growth and faster absolute and fractional juvenile growth. Relative feed intake in juveniles was increased in offspring from larger litters, and increased neonatal growth also predicted hyperphagia in juveniles. Rapid neonatal growth also correlated with increased visceral adiposity in adult males, but not females, suggesting sex-specific programming of postnatal phenotype. Thus, the spontaneously IUGR guinea pig exhibits key features of human IUGR including neonatal catch-up growth, postnatal hyperphagia and increased fat deposition (Chapter 2). To enable further study of the effects of litter size and neonatal growth on insulin sensitivity, methodology for the hyperinsulinaemic euglycaemic clamp (HEC) was validated for use in the guinea pig. The dose-response curve for whole-body glucose uptake using recombinant human insulin was characterised and HECs with D-[3-3H]-glucose infusion were performed to characterise insulin sensitivities of whole body glucose uptake and partitioning of glucose metabolism in males and females at ~half maximal and near maximal insulin doses. Insulin infusion at 7.5 mU.min-1.kg-1 increased glucose utilisation and storage, while suppressing glucose production, while insulin at 30 mU.min-1.kg-1 also increased the rate of glycolysis. Fasting plasma glucose, metabolic clearance of insulin and rates of glucose utilisation, storage and production during insulin stimulation were higher in female than male guinea pigs, but insulin sensitivity of these and whole body glucose uptake did not differ between sexes (Chapter 3). HEC was then used to assess whole body insulin sensitivity and partitioned glucose metabolism in young adult offspring from varying litter sizes. In males, insulin sensitivities of whole body glucose uptake and glucose utilisation correlated positively, while that of endogenous glucose production tended to correlate positively with birth weight, and these associations were independent of neonatal catch-up growth, adult adiposity and muscle mass. Whole body and partitioned glucose metabolism in young adult females were not related to birth weight, however, the insulin sensitivity of endogenous glucose production correlated negatively with neonatal catch-up growth independently of birth weight. These results suggest a contribution of intrinsic deficits in skeletal muscle and liver to sex-specific perinatal programming of insulin resistance in this species (Chapter 4). Overall, these studies demonstrate that increasing litter size in the guinea pig results in asymmetrical IUGR. The spontaneously growth restricted guinea pig exhibits sex-specific programming of postnatal growth, appetite, adiposity and insulin sensitivity, occurring primarily in males, not unlike that in humans and other animal models. This therefore provides a model for investigating the causal mechanisms and effects of ageing on the perinatal programming of obesity and insulin resistance in liver and skeletal muscle.
Thesis (Ph.D.) -- University of Adelaide, Adelaide Medical School, 2017