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161. Insulin acutely inhibits intestinal lipoprotein secretion in humans in part by suppressing plasma free fatty acids.
作者: Mirjana Pavlic.;Changting Xiao.;Linda Szeto.;Bruce W Patterson.;Gary F Lewis.
来源: Diabetes. 2010年59卷3期580-7页
Intestinal lipoprotein production has recently been shown to be increased in insulin resistance, but it is not known whether it is regulated by insulin in humans. Here, we investigated the effect of acute hyperinsulinemia on intestinal (and hepatic) lipoprotein production in six healthy men in the presence and absence of concomitant suppression of plasma free fatty acids (FFAs).
162. Metabolic changes following a 1-year diet and exercise intervention in patients with type 2 diabetes.
作者: Jeanine B Albu.;Leonie K Heilbronn.;David E Kelley.;Steven R Smith.;Koichiro Azuma.;Evan S Berk.;F Xavier Pi-Sunyer.;Eric Ravussin.; .
来源: Diabetes. 2010年59卷3期627-33页
To characterize the relationships among long-term improvements in peripheral insulin sensitivity (glucose disposal rate [GDR]), fasting glucose, and free fatty acids (FFAs) and concomitant changes in weight and adipose tissue mass and distribution induced by lifestyle intervention in obese individuals with type 2 diabetes.
163. Sympathetic neural adaptation to hypocaloric diet with or without exercise training in obese metabolic syndrome subjects.
作者: Nora E Straznicky.;Elisabeth A Lambert.;Paul J Nestel.;Mariee T McGrane.;Tye Dawood.;Markus P Schlaich.;Kazuko Masuo.;Nina Eikelis.;Barbora de Courten.;Justin A Mariani.;Murray D Esler.;Florentia Socratous.;Reena Chopra.;Carolina I Sari.;Eldho Paul.;Gavin W Lambert.
来源: Diabetes. 2010年59卷1期71-9页
Sympathetic nervous system (SNS) overactivity contributes to the pathogenesis and target organ complications of obesity. This study was conducted to examine the effects of lifestyle interventions (weight loss alone or together with exercise) on SNS function.
164. Impact of the PPAR-gamma2 Pro12Ala polymorphism and ACE inhibitor therapy on new-onset microalbuminuria in type 2 diabetes: evidence from BENEDICT.
作者: Salvatore De Cosmo.;Nicola Motterlini.;Sabrina Prudente.;Fabio Pellegrini.;Roberto Trevisan.;Antonio Bossi.;Giuseppe Remuzzi.;Vincenzo Trischitta.;Piero Ruggenenti.; .
来源: Diabetes. 2009年58卷12期2920-9页
Cross-sectional studies found less microalbuminuria in type 2 diabetic patients with the Ala12 allele of the peroxisome proliferator-activated receptor-gamma2 (PPAR-gamma2) Pro12Ala polymorphism. We prospectively evaluated the association between Pro12Ala polymorphism (rs1801282) and new-onset microalbuminuria.
165. Low-fat versus low-carbohydrate weight reduction diets: effects on weight loss, insulin resistance, and cardiovascular risk: a randomized control trial.
作者: Una Bradley.;Michelle Spence.;C Hamish Courtney.;Michelle C McKinley.;Cieran N Ennis.;David R McCance.;Jane McEneny.;Patrick M Bell.;Ian S Young.;Steven J Hunter.
来源: Diabetes. 2009年58卷12期2741-8页
Low-fat hypocaloric diets reduce insulin resistance and prevent type 2 diabetes in those at risk. Low-carbohydrate, high-fat diets are advocated as an alternative, but reciprocal increases in dietary fat may have detrimental effects on insulin resistance and offset the benefits of weight reduction.
166. Effects of differing antecedent increases of plasma cortisol on counterregulatory responses during subsequent exercise in type 1 diabetes.
Antecedent hypoglycemia can blunt neuroendocrine and autonomic nervous system responses to next-day exercise in type 1 diabetes. The aim of this study was to determine whether antecedent increase of plasma cortisol is a mechanism responsible for this finding.
167. Effect of homocysteine-lowering treatment with folic Acid and B vitamins on risk of type 2 diabetes in women: a randomized, controlled trial.
作者: Yiqing Song.;Nancy R Cook.;Christine M Albert.;Martin Van Denburgh.;JoAnn E Manson.
来源: Diabetes. 2009年58卷8期1921-8页
Homocysteinemia may play an etiologic role in the pathogenesis of type 2 diabetes by promoting oxidative stress, systemic inflammation, and endothelial dysfunction. We investigated whether homocysteine-lowering treatment by B vitamin supplementation prevents the risk of type 2 diabetes.
168. Muscle microvascular dysfunction in central obesity is related to muscle insulin insensitivity but is not reversed by high-dose statin treatment.
作者: Geraldine F Clough.;Magdalena Turzyniecka.;Lara Walter.;Andrew J Krentz.;Sarah H Wild.;Andrew J Chipperfield.;John Gamble.;Christopher D Byrne.
来源: Diabetes. 2009年58卷5期1185-91页
To test the hypotheses that decreased insulin-mediated glucose disposal in muscle is associated with a reduced muscle microvascular exchange capacity (Kf) and that 6 months of high-dose statin therapy would improve microvascular function in people with central obesity.
169. Antecedent hypoglycemia impairs autonomic cardiovascular function: implications for rigorous glycemic control.
作者: Gail K Adler.;Istvan Bonyhay.;Hannah Failing.;Elizabeth Waring.;Sarah Dotson.;Roy Freeman.
来源: Diabetes. 2009年58卷2期360-6页
Glycemic control decreases the incidence and progression of diabetic complications but increases the incidence of hypoglycemia. Hypoglycemia can impair hormonal and autonomic responses to subsequent hypoglycemia. Intensive glycemic control may increase mortality in individuals with type 2 diabetes at high risk for cardiovascular complications. We tested the hypothesis that prior exposure to hypoglycemia leads to impaired cardiovascular autonomic function.
170. Physical inactivity differentially alters dietary oleate and palmitate trafficking.
作者: Audrey Bergouignan.;Guy Trudel.;Chantal Simon.;Angèle Chopard.;Dale A Schoeller.;Iman Momken.;Susanne B Votruba.;Michel Desage.;Graham C Burdge.;Guillemette Gauquelin-Koch.;Sylvie Normand.;Stéphane Blanc.
来源: Diabetes. 2009年58卷2期367-76页
Obesity and diabetes are characterized by the incapacity to use fat as fuel. We hypothesized that this reduced fat oxidation is secondary to a sedentary lifestyle.
171. Portal vein glucose sensors do not play a major role in modulating physiological responses to insulin-induced hypoglycemia in humans.
作者: Paolo Rossetti.;Francesca Porcellati.;Paola Lucidi.;Natalia Busciantella Ricci.;Paola Candeloro.;Patrizia Cioli.;Fausto Santeusanio.;Geremia B Bolli.;Carmine G Fanelli.
来源: Diabetes. 2009年58卷1期194-202页
Experimental data from animal studies indicate that portal vein glucose sensors play a key role in the responses to slow-fall hypoglycemia. However, their role in modulating these responses in humans is not well understood. The aim of the present study was to examine in humans the potential role of portal vein glucose sensors in physiological responses to insulin-induced hypoglycemia mimicking the slow fall of insulin-treated diabetic subjects.
172. Effects of the selective serotonin reuptake inhibitor fluoxetine on counterregulatory responses to hypoglycemia in individuals with type 1 diabetes.
作者: Vanessa J Briscoe.;Andrew C Ertl.;Donna B Tate.;Stephen N Davis.
来源: Diabetes. 2008年57卷12期3315-22页
Previous work has demonstrated that chronic administration of the serotonin reuptake inhibitor (SSRI) fluoxetine augments counterregulatory responses to hypoglycemia in healthy humans. However, virtually no information exists regarding the effects of fluoxetine on integrated physiological counterregulatory responses during hypoglycemia in type 1 diabetes. Therefore, the specific aim of this study was to test the hypothesis that 6-week use of the SSRI fluoxetine would amplify autonomic nervous system (ANS) counterregulatory responses to hypoglycemia in individuals with type 1 diabetes.
173. Correction of HDL dysfunction in individuals with diabetes and the haptoglobin 2-2 genotype.
作者: Rabea Asleh.;Shany Blum.;Shiri Kalet-Litman.;Jonia Alshiek.;Rachel Miller-Lotan.;Roy Asaf.;Wasseem Rock.;Michael Aviram.;Uzi Milman.;Chen Shapira.;Zaid Abassi.;Andrew P Levy.
来源: Diabetes. 2008年57卷10期2794-800页
Pharmacogenomics is a key component of personalized medicine. The Israel Cardiovascular Events Reduction with Vitamin E Study, a prospective placebo-controlled study, recently demonstrated that vitamin E could dramatically reduce CVD in individuals with diabetes and the haptoglobin (Hp) 2-2 genotype (40% of diabetic individuals). However, because of the large number of clinical trials that failed to demonstrate benefit from vitamin E coupled with the lack of a mechanistic explanation for why vitamin E should be beneficial only in diabetic individuals with the Hp 2-2 genotype, enthusiasm for this pharmacogenomic paradigm has been limited. In this study, we sought to provide such a mechanistic explanation based on the hypothesis that the Hp 2-2 genotype and diabetes interact to promote HDL oxidative modification and dysfunction.
174. Cholinergic regulation of ghrelin and peptide YY release may be impaired in obesity.
作者: Christina Maier.;Michaela Riedl.;Greisa Vila.;Peter Nowotny.;Michael Wolzt.;Martin Clodi.;Bernhard Ludvik.;Anton Luger.
来源: Diabetes. 2008年57卷9期2332-40页
Ghrelin and peptide YY (PYY) are both hormones derived from the gastrointestinal tract involved in appetite regulation. The cholinergic part of the vagal nerve is involved in the regulation of glucose and insulin. The aim of this study was to examine the effects of the cholinergic antagonist atropine on ghrelin, PYY, glucose, and insulin under basal conditions and after meal ingestion in lean and obese subjects.
175. Effects of a selective serotonin reuptake inhibitor, fluoxetine, on counterregulatory responses to hypoglycemia in healthy individuals.
作者: Vanessa J Briscoe.;Andrew C Ertl.;Donna B Tate.;Sheila Dawling.;Stephen N Davis.
来源: Diabetes. 2008年57卷9期2453-60页
Hypoglycemia commonly occurs in intensively-treated diabetic patients. Repeated hypoglycemia blunts counterregulatory responses, thereby increasing the risk for further hypoglycemic events. Currently, physiologic approaches to augment counterregulatory responses to hypoglycemia have not been established. Therefore, the specific aim of this study was to test the hypothesis that 6 weeks' administration of the selective serotonin reuptake inhibitor (SSRI) fluoxetine would amplify autonomic nervous system (ANS) and neuroendocrine counterregulatory mechanisms during hypoglycemia.
176. Impact of diabetes susceptibility loci on progression from pre-diabetes to diabetes in at-risk individuals of the diabetes prevention trial-type 1 (DPT-1).
作者: Vincent Butty.;Christopher Campbell.;Diane Mathis.;Christophe Benoist.; .
来源: Diabetes. 2008年57卷9期2348-59页
The unfolding of type 1 diabetes involves a number of steps: defective immunological tolerance, priming of anti-islet autoimmunity, and destruction of insulin-producing beta-cells. A number of genetic loci contribute to susceptibility to type 1 diabetes, but it is unclear which stages of the disease are influenced by the different loci. Here, we analyzed the frequency of type 1 diabetes-risk alleles among individuals from the Diabetes Prevention Trial-Type 1 (DPT-1) clinical trial, which tested a preventive effect of insulin in at-risk relatives of diabetic individuals, all of which presented with autoimmune manifestations but only one-third of which eventually progressed to diabetes.
177. Mitochondrial capacity in skeletal muscle is not stimulated by weight loss despite increases in insulin action and decreases in intramyocellular lipid content.
作者: Frederico G S Toledo.;Elizabeth V Menshikova.;Koichiro Azuma.;Zofia Radiková.;Carol A Kelley.;Vladimir B Ritov.;David E Kelley.
来源: Diabetes. 2008年57卷4期987-94页
In obesity and type 2 diabetes, exercise combined with weight loss increases skeletal muscle mitochondrial capacity. It remains unclear whether mitochondrial capacity increases because of weight loss, improvements in insulin resistance, or physical training. In this study, we examined the effects of an intervention of weight loss induced by diet and compared these with those of a similar intervention of weight loss by diet with exercise. Both are known to improve insulin resistance, and we tested the hypothesis that physical activity, rather than improved insulin resistance, is required to increase mitochondrial capacity of muscle.
178. Effect of glycemic exposure on the risk of microvascular complications in the diabetes control and complications trial--revisited.
作者: John M Lachin.;Saul Genuth.;David M Nathan.;Bernard Zinman.;Brandy N Rutledge.; .
来源: Diabetes. 2008年57卷4期995-1001页
The Diabetes Control and Complications Trial (Diabetes 44:968-983, 1995) presented statistical models suggesting that subjects with similar A1C levels had a higher risk of retinopathy progression in the conventional treatment group than in the intensive treatment group. That analysis has been cited to support the hypothesis that specific patterns of glucose variation, in particular postprandial hyperglycemia, contribute uniquely to an increased risk of microvascular complications above and beyond that explained by the A1C level.
179. Different brain responses to hypoglycemia induced by equipotent doses of the long-acting insulin analog detemir and human regular insulin in humans.
作者: Paolo Rossetti.;Francesca Porcellati.;Natalia Busciantella Ricci.;Paola Candeloro.;Patrizia Cioli.;Geremia B Bolli.;Carmine G Fanelli.
来源: Diabetes. 2008年57卷3期746-56页
The acylated long-acting insulin analog detemir is more lipophilic than human insulin and likely crosses the blood-to-brain barrier more easily than does human insulin. The aim of these studies was to assess the brain/hypothalamus responses to euglycemia and hypoglycemia in humans during intravenous infusion of equipotent doses of detemir and human insulin.
180. Activation of peroxisome proliferator-activated receptor (PPAR)delta promotes reversal of multiple metabolic abnormalities, reduces oxidative stress, and increases fatty acid oxidation in moderately obese men.
作者: Ulf Risérus.;Dennis Sprecher.;Tony Johnson.;Eric Olson.;Sandra Hirschberg.;Aixue Liu.;Zeke Fang.;Priti Hegde.;Duncan Richards.;Leli Sarov-Blat.;Jay C Strum.;Samar Basu.;Jane Cheeseman.;Barbara A Fielding.;Sandy M Humphreys.;Theodore Danoff.;Niall R Moore.;Peter Murgatroyd.;Stephen O'Rahilly.;Pauline Sutton.;Tim Willson.;David Hassall.;Keith N Frayn.;Fredrik Karpe.
来源: Diabetes. 2008年57卷2期332-9页
Pharmacological use of peroxisome proliferator-activated receptor (PPAR)delta agonists and transgenic overexpression of PPARdelta in mice suggest amelioration of features of the metabolic syndrome through enhanced fat oxidation in skeletal muscle. We hypothesize a similar mechanism operates in humans.
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