Long-term use of nicotine gum is associated with hyperinsulinemia and insulin resistance

1997 ◽  
Vol 6 (2) ◽  
pp. 88
Keyword(s):  
Insulin Resistance ◽  
Nicotine Gum

Long-term Use of Nicotine Gum Is Associated With Hyperinsulinemia and Insulin Resistance

Circulation ◽  
1996 ◽  
Vol 94 (5) ◽  
pp. 878-881 ◽  
Author(s):  
Bjo¨rn Eliasson ◽  
Marja-Riitta Taskinen ◽  
Ulf Smith
Keyword(s):  
Insulin Resistance ◽  
Nicotine Gum

scholarly journals Association of Long-term Change in Waist Circumference With Insulin Resistance

Obesity ◽  
2010 ◽  
Vol 18 (2) ◽  
pp. 370-376 ◽  
Author(s):  
Kyong Park ◽  
Duk-Hee Lee ◽  
Darin J. Erickson ◽  
John H. Himes ◽  
James M. Shikany ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Waist Circumference ◽  
Term Change

scholarly journals Interaction of physical activity and diet: implications for insulin-glucose dynamics

1999 ◽  
Vol 2 (3a) ◽  
pp. 363-368 ◽  
Author(s):  
Jean-Jacques Grimm
Keyword(s):  
Insulin Resistance ◽  
Cardiovascular Risk ◽  
Fatty Acid ◽  
Glycogen Synthase ◽  
Insulin Resistance Syndrome ◽  
Low Fat ◽  
Exercise Interventions ◽  
High Carbohydrate ◽  
Fat Diets

AbstractIn Western countries 25–35% of the population have insulin resistance syndrome characteristics.The defects most likely to explain the insulin resistance of the insulin resistance syndrome include: 1) the glucose transport system of skeletal muscle (GLUT-4) and its different signalling proteins and enzymes; 2) glucose phosphorylation by hexokinase; 3) glycogen synthase activity and 4) competition between glucose and fatty acid oxidation (glucose-fatty acid cycle).High carbohydrate/low fat diets deteriorate insulin sensitivity on the short term. Howewer, on the long term, high fat/low carbohydrate diets have a lower satiating power, induce low leptin levels and eventually lead to higher energy consumption, obesity and more insulin resistance. Moderately high-carbohydrate (45–55% of the daily calories)/low-fat diets seem to be a good choice with regard to the prevention of diabetes and cardiovascular risk factors as far as the carbohydrates are rich in fibers.Long-term interventions with regular exercise programs show a 1/3 decrease in the appearance of overt diabetes in glucose intolerant subjects. Furthermore, diet and exercise interventions "normalise" the mortality rate of patients with impared glucose tolerance.Therefore, moderately high carbohydrate/low fat diets are most likely to prevent obesity and type 2 diabetes. Triglycerides should be monitored and, in some cases, a part of the carbohydrates could be replaced by fat rich in monounsaturated fatty acids. However, total caloric intake is of utmost importance, as weight gain is the major determinant for the onset of insulin resistance and glucose intolerance.Regular (when possible daily) exercise, decreases cardiovascular risk. With regard to insulin resistance, resistance training seems to offer some advantages over aerobic endurance activities.

Effect of insulin resistance associated with compensatory hyperinsulinemia on the long-term prognosis in patients with vasospastic angina

2013 ◽  
Vol 167 (5) ◽  
pp. 2222-2227 ◽  
Author(s):  
Akihiro Nakagomi ◽  
Yoshiyuki Saiki ◽  
Munenori Kosugi ◽  
Keiichi Kohashi ◽  
Yoshitomo Yoshikawa ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vasospastic Angina ◽  
Long Term Prognosis

scholarly journals Central Insulin Signaling Is Attenuated by Long-Term Insulin Exposure via Insulin Receptor Substrate-1 Serine Phosphorylation, Proteasomal Degradation, and Lysosomal Insulin Receptor Degradation

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 75-84 ◽  
Author(s):  
Christopher M. Mayer ◽  
Denise D. Belsham
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptor ◽  
Insulin Signaling ◽  
Time Course ◽  
Proteasomal Degradation ◽  
Serine Phosphorylation ◽  
Neuronal Function ◽  
Protein Levels ◽  
Phosphorylated Akt

Abstract Central insulin signaling is critical for the prevention of insulin resistance. Hyperinsulinemia contributes to insulin resistance, but it is not yet clear whether neurons are subject to cellular insulin resistance. We used an immortalized, hypothalamic, clonal cell line, mHypoE-46, which exemplifies neuronal function and expresses the components of the insulin signaling pathway, to determine how hyperinsulinemia modifies neuronal function. Western blot analysis indicated that prolonged insulin treatment of mHypoE-46 cells attenuated insulin signaling through phospho-Akt. To understand the mechanisms involved, time-course analysis was performed. Insulin exposure for 4 and 8 h phosphorylated Akt and p70-S6 kinase (S6K1), whereas 8 and 24 h treatment decreased insulin receptor (IR) and IR substrate 1 (IRS-1) protein levels. Insulin phosphorylation of S6K1 correlated with IRS-1 ser1101 phosphorylation and the mTOR-S6K1 pathway inhibitor rapamycin prevented IRS-1 serine phosphorylation. The proteasomal inhibitor epoxomicin and the lysosomal pathway inhibitor 3-methyladenine prevented the degradation of IRS-1 and IR by insulin, respectively, and pretreatment with rapamycin, epoxomicin, or 3-methyladenine prevented attenuation of insulin signaling by long-term insulin exposure. Thus, a sustained elevation of insulin levels diminishes neuronal insulin signaling through mTOR-S6K1-mediated IRS-1 serine phosphorylation, proteasomal degradation of IRS-1 and lysosomal degradation of the IR.

Insulin resistance induced by long-term sleep deprivation in rhesus macaques can be attenuated by Bifidobacterium

2021 ◽  
Author(s):  
Ying Zhao ◽  
Yan Shu ◽  
Ning Zhao ◽  
Zili Zhou ◽  
Xiong Jia ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Circadian Rhythm ◽  
Blood Glucose ◽  
Glucose Metabolism ◽  
Sleep Deprivation ◽  
Rhesus Macaques ◽  
Intravenous Glucose ◽  
Increased Risk ◽  
The Impact

Long-term sleep deprivation (SD) is a bad lifestyle habit, especially among specific occupational practitioners, characterized by circadian rhythm misalignment and abnormal sleep/wake cycles. SD is closely associated with an increased risk of metabolic disturbance, particularly obesity and insulin resistance. The incretin hormone, glucagon-like peptide-1 (GLP-1), is a critical insulin release determinant secreted by the intestinal L-cell upon food intake. Besides, the gut microbiota participates in metabolic homeostasis and regulates GLP-1 release in a circadian rhythm manner. As a commonly recognized intestinal probiotic, Bifidobacterium has various clinical indications regarding its curative effect. However, few studies have investigated the effect of Bifidobacterium supplementation on sleep disorders. In the present study, we explored the impact of long-term SD on the endocrine metabolism of rhesus monkeys and determined the effect of Bifidobacterium supplementation on the SD-induced metabolic status. Lipids concentrations, body weight, fast blood glucose, and insulin levels increased after SD. Furthermore, after two months of long-term SD, the intravenous glucose tolerance test (iVGTT) showed that the glucose metabolism was impaired and the insulin sensitivity decreased. Moreover, one month of Bifidobacterium oral administration significantly reduced blood glucose and attenuated insulin resistance in rhesus macaques. Overall, our results suggested that Bifidobacterium might be used to alleviate SD-induced aberrant glucose metabolism and improve insulin resistance. Also, it might help in better understanding the mechanisms governing the beneficial effects of Bifidobacterium.

scholarly journals Hyperglycemia in the Posttransplant Period: NODAT vs Posttransplant Diabetes Mellitus

2018 ◽  
Vol 2 (11) ◽  
pp. 1314-1319 ◽  
Author(s):  
Suruchi Gupta ◽  
Teresa Pollack ◽  
Candice Fulkerson ◽  
Kathleen Schmidt ◽  
Diana Johnson Oakes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Liver Transplant ◽  
Controlled Trial ◽  
Organ Transplant ◽  
Long Term Outcomes ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Persistent Hyperglycemia

Abstract Objective To characterize the types of hyperglycemia that occur up to 1 year following liver transplant and to clarify the nomenclature for posttransplant hyperglycemia. Design We analyzed 1-year glycemic follow-up data in 164 patients who underwent liver transplant and who had been enrolled in a randomized controlled trial comparing moderate to intensive insulin therapy to determine if patients had preexisting known diabetes, transient hyperglycemia, persistent hyperglycemia, or new-onset diabetes after transplantation (NODAT). Results Of 119 patients with posttransplant hyperglycemia following hospital discharge, 49 had preexisting diabetes, 5 had insufficient data for analysis, 48 had transient hyperglycemia (16 resolved within 30 days and 32 resolved between 30 days and 1 year), 13 remained persistently hyperglycemic out to 1 year and most likely had preexisting diabetes that had not been diagnosed or insulin resistance/insulinopenia prior to transplant, and 4 had NODAT (i.e., patients with transient hyperglycemia after transplant that resolved but then later truly developed sustained hyperglycemia, meeting criteria for diabetes). Conclusions Distinct categories of patients with hyperglycemia following organ transplant include known preexisting diabetes, persistent hyperglycemia (most likely unknown preexisting diabetes or insulin resistance/insulinopenia), transient hyperglycemia, and NODAT. Those with preexisting diabetes for many years prior to transplant may well have very different long-term outcomes compared with those with true NODAT. Therefore, it would be prudent to classify patients more carefully. Long-term outcome studies are needed to determine if patients with true NODAT have the same poor prognosis as patients with preexisting diabetes (diagnosed and undiagnosed) undergoing transplant.

Effect of Long-Term Exercise Training on lncRNAs Expression in the Vascular Injury of Insulin Resistance

2018 ◽  
Vol 11 (6) ◽  
pp. 459-469 ◽  
Author(s):  
Suixin Liu ◽  
Fan Zheng ◽  
Ying Cai ◽  
Wenliang Zhang ◽  
Yaoshan Dun
Keyword(s):  
Insulin Resistance ◽  
Exercise Training ◽  
Vascular Injury

scholarly journals Chronic caffeine intake decreases circulating catecholamines and prevents diet-induced insulin resistance and hypertension in rats

2011 ◽  
Vol 107 (1) ◽  
pp. 86-95 ◽  
Author(s):  
Silvia V. Conde ◽  
Tiago Nunes da Silva ◽  
Constancio Gonzalez ◽  
Miguel Mota Carmo ◽  
Emilia C. Monteiro ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Gain ◽  
Visceral Fat ◽  
Tolerance Test ◽  
Caffeine Intake ◽  
Insulin Tolerance ◽  
Hepatic Glutathione ◽  
Chronic Caffeine ◽  
High Sucrose

We tested the hypothesis that long-term caffeine intake prevents the development of insulin resistance and hypertension in two pathological animal models: the high-fat (HF) and the high-sucrose (HSu) diet rat. We used six groups of animals: control; caffeine-treated (Caff; 1 g/l in drinking water during 15 d); HF; caffeine-treated HF (HFCaff); HSu; caffeine-treated HSu (HSuCaff). Insulin sensitivity was assessed using the insulin tolerance test. Blood pressure, weight gain, visceral fat, hepatic glutathione, plasma caffeine, insulin and NO, and serum NEFA and catecholamines were measured. Caffeine reversed insulin resistance and hypertension induced by both the HF and HSu diets. In the HF-fed animals caffeine treatment restored fasting insulin levels to control values and reversed increased weight gain and visceral fat mass. In the HSu group, caffeine reversed fasting hyperglycaemia and restored NEFA to control values. There were no changes either in plasma NO or in hepatic glutathione levels. In contrast, caffeine totally prevented the increase in serum catecholamines induced by HF and HSu diets. To test the hypothesis that inhibition of the sympathetic nervous system prevents the development of diet-induced insulin resistance we administered carvedilol, an antagonist of β1, β2 and also α1 adrenoceptors, to HF and HSu rats. Carvedilol treatment fully prevented diet-induced insulin resistance and hypertension, mimicking the effect of caffeine. We concluded that long-term caffeine intake prevented the development of insulin resistance and hypertension in HF and HSu models and that this effect was related to a decrease in circulating catecholamines.

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