Vanadium compounds have been shown to have insulin-like properties in rats and non-insulin-dependent diabetic humans. The purpose of the present study was to examine whether the effects of acute and short-term administration of vanadyl sulphate (VS) on insulin sensitivity also exist in healthy active individuals. Five male and 2 female participants (age: 24.9 ± 1.5 years; height: 176.1 ± 2.9 cm; body mass: 70.1 ± 2.9 kg) underwent 3 oral glucose tolerance tests (OGTT). The first OGTT was performed to obtain a baseline index of insulin sensitivity (ISI). On the night preceding the second OGTT, participants ingested 100 mg of VS, and the acute effects of VS on ISI were examined. For the next 6 days, participants were instructed to ingest 50 mg of VS twice daily, and a final OGTT was performed on day 7 to determine the short-term effects of VS on ISI. No differences were found in fasting plasma glucose and insulin concentrations after VS administration. Furthermore, ISI after 1 day and 7 days of VS administration was not different compared with baseline ISI (4.8±0.1 vs. 4.7±0.1 vs. 4.7 ± 0.1, respectively). These results demonstrate that there are no acute and short-term effects of VS administration on insulin sensitivity in healthy humans.
Roy L.P.G. Jentjens and Asker E. Jeukendrup
Craig A. Horswill, William B. Zipf, C. Lawrence Kien and E. Bowie Kahle
Insulin is an anabolic hormone with stimulatory effects on glucose and amino acid uptake, possibly protein synthesis, and bone growth, and inhibitory effects on protein breakdown. The precise role of insulin in the growth of healthy children is unclear, but two clinical models can be examined to illustrate insulin’s potential role in the growth of children. The cystic fibrosis (CF) patient, who exhibits poor linear growth and low lean body mass, may exhibit inadequate insulin secretion or impaired insulin action. The obese child typically has an excess of peripheral insulin, an associated acceleration of linear growth, and an accretion of lean body mass and adipose tissue. Speculation is offered on the putative role of exercise in affecting insulin action and secretion, which in turn could impact growth in children with CF or obesity.
Laís Monteiro Rodrigues Loureiro, Caio Eduardo Gonçalves Reis and Teresa Helena Macedo da Costa
, caffeic acid, chlorogenic acid, trigonelline, secoisolariciresinol, and oxokahweol (10 −12 –10 −6 M for 60 min); cafestol and caffeic acid (10 −12 –10 −8 M for 72 hr) Cafestol and caffeic acid acutely and chronically increased insulin secretion from beta cells. Cafestol increased glucose uptake in
Andrzej Gawrecki, Aleksandra Araszkiewicz, Agnieszka Szadkowska, Grzegorz Biegański, Jan Konarski, Katarzyna Domaszewska, Arkadiusz Michalak, Bogda Skowrońska, Anna Adamska, Dariusz Naskręt, Przemysława Jarosz-Chobot, Agnieszka Szypowska, Tomasz Klupa and Dorota Zozulińska-Ziółkiewicz
knowledge about behavior during physical activity ( 17 ). Thanks to the progress and application of new technologies in the treatment of diabetes; these barriers have been largely overcome in the last decade ( 31 ). The use of analog insulins, insulin pumps, and continuous glucose measurement systems has
Rachel B. Parks, Hector F. Angus, Douglas S. King and Rick L. Sharp
synergistic actions of insulin and muscle contractions stimulated GLUT4 translocation until counterregulatory hormones normalized blood glucose by ∼30 min into exercise ( Defronzo et al., 1981 ; Hargreaves et al., 1987 ). However, subsequent studies could not replicate the results, instead finding
Susan Sullivan Glenney, Derrick Paul Brockemer, Andy C. Ng, Michael A. Smolewski, Vladimir M. Smolgovskiy and Adam S. Lepley
effects of exercise training on cardiovascular health. Traditional serum biomarkers, such as total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), glucose, C-reactive protein (CRP), insulin, and triglyceride levels, have been used to study the effects of exercise interventions
Emma L. Sweeney, Daniel J. Peart, Irene Kyza, Thomas Harkes, Jason G. Ellis and Ian H. Walshe
al., 2006 ). Experimental studies demonstrate impaired glucose control following sleep restriction (SR; Knutson et al., 2007 ), with a single night of restriction reducing whole-body insulin sensitivity by 20% ( Donga et al., 2010 ). The proposed mechanisms underlying impaired glucose regulation following
Luke R. Bucci, James F. Hickson Jr., Ira Wolinsky and James M. Pivarnik
Ornithine supplementation has gained popularity with athletes because of its alleged potential to release anabolic hormones, factors governing skeletal muscle hypertrophy. Three female and nine male bodybuilders sewed as subjects in a study to test the effectiveness of oral ornithine in bringing about the release of insulin, an anabolic hormone. After an overnight fast, subjects were administered 40, 100, or 170 mg·kg−1 L-ornithine.HC1 by mouth in a random fashion on three consecutive Saturday mornings. Blood samples were drawn at baseline (T=O), 45, and 90 min afterward. Serum ornithine levels were elevated (p~0.01) at T=45 and 90 min for all three dosage levels. However, serum insulin did not change from baseline levels at any dose of ornithine. The present findings show that ornithine is not an insulin secretagogue.
Isao Saito, Koutatsu Maruyama, Tadahiro Kato, Yasunori Takata, Kiyohide Tomooka, Ryoichi Kawamura, Yuichi Uesugi, Yoshihiko Naito, Haruhiko Osawa and Takeshi Tanigawa
Physical inactivity increases the risk of cardiovascular disease (CVD) incidence, CVD mortality, and all-cause mortality in association with weight gain, dyslipidemia, and development of metabolic syndrome, diabetes, and hypertension. 1 – 3 In addition to these findings, the presence of insulin
G. Lynis Dohm
We previously reported that insulin resistance in skeletal muscle of obese individuals was associated with decreases in insulin signal transduction and tyrosine kinase activity of the insulin receptor. Herein is reviewed the recently published data supporting the hypothesis that protein kinase C (PKC) phosphorylates the insulin receptor on serine/threonine residues to decrease tyrosine kinase activity and cause insulin resistance. Treatment of insulin receptors from obese subjects with alkaline phosphatase restored tyrosine kinase activity, suggesting that the reduced activity was a result of hyperphosphorylation of the receptor. Incubating human muscle fiber strips with PKC inhibitors restored insulin action in muscle of obese patients, while activating PKC with a phorbol ester caused insulin resistance in muscle from lean control patients. The beta isoform of PKC was elevated in muscle of obese, insulin-resistant patients. These data are consistent with the hypothesis that elevated PKC activity may cause insulin resistance by phosphorylating the insulin receptor to decrease tyrosine kinase activity.