scholarly journals Genetic susceptibility to diabetes and long-term improvement of insulin resistance and β cell function during weight loss: the Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial

2016 ◽  
Vol 104 (1) ◽  
pp. 198-204 ◽  
Author(s):  
Tao Huang ◽  
Sylvia H Ley ◽  
Yan Zheng ◽  
Tiange Wang ◽  
George A Bray ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Genetic Susceptibility ◽  
Cell Function ◽  
Β Cell ◽  
Β Cell Function ◽  
Dietary Strategies

scholarly journals Long-Term Effects of Central Leptin and Resistin on Body Weight, Insulin Resistance, and β-Cell Function and Mass by the Modulation of Hypothalamic Leptin and Insulin Signaling

Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 445-454 ◽  
Author(s):  
Sunmin Park ◽  
Sang Mee Hong ◽  
So Ra Sung ◽  
Hye Kyung Jung
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Insulin Signaling ◽  
Cell Function ◽  
Cell Mass ◽  
Diabetic Rats ◽  
Β Cell ◽  
Serum Leptin ◽  
Β Cell Function

To determine the long-term effect of central leptin and resistin on energy homeostasis, peripheral insulin resistance, and β-cell function and mass, intracerebroventricular (ICV) infusion of leptin (3 ng/h), resistin (80 ng/h), leptin plus resistin, and cerebrospinal fluid (control) was conducted by means of an osmotic pump for 4 wk on normal rats and 90% pancreatectomized diabetic rats fed 40% fat-energy diets. Overall, the effects were greater in diabetic rats than normal rats. Leptin infusion, causing a significant reduction in food intake, decreased body weight and epididymal fat. However, resistin and leptin plus resistin reduced epididymal fat with decreased serum leptin levels in comparison with the control. Unlike serum leptin, only resistin infusion lowered serum resistin levels. Central leptin increased glucose infusion rates during euglycemic hyperinsulinemic clamp and suppressed hepatic glucose production in the hyperinsulinemic state in comparison with the control. However, central leptin did not affect glucose-stimulated insulin secretion and β-cell mass. Central resistin infusion also increased peripheral insulin sensitivity, but not as much as leptin. Unlike leptin, resistin significantly increased first-phase insulin secretion during hyperglycemic clamp and β-cell mass by augmenting β-cell proliferation. These metabolic changes were associated with hypothalamic leptin and insulin signaling. ICV infusion of leptin potentiated signal transducer and activator of transcription 3 phosphorylation and attenuated AMP kinase in the hypothalamus, but resistin had less potent effects than leptin. Leptin enhanced insulin signaling by potentiating IRS2→Akt pathways, whereas resistin activated Akt without augmenting insulin receptor substrate 2 phosphorylation. In conclusion, long-term ICV infusion of leptin and resistin independently improved energy and glucose homeostasis by modulating in different ways hypothalamic leptin and insulin signaling.

scholarly journals Effects of Low-Carbohydrate versus Mediterranean Diets on Weight Loss, Glucose Metabolism, Insulin Kinetics and β-Cell Function in Morbidly Obese Individuals

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1345
Author(s):  
Domenico Tricò ◽  
Diego Moriconi ◽  
Rossana Berta ◽  
Simona Baldi ◽  
Alfredo Quinones-Galvan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Weight Loss ◽  
Cell Function ◽  
Insulin Clearance ◽  
Morbidly Obese ◽  
Β Cell ◽  
Carbohydrate Diet ◽  
Low Carbohydrate Diet ◽  
Low Carbohydrate ◽  
Β Cell Function

Low-calorie Mediterranean-style or low-carbohydrate dietary regimens are widely used nutritional strategies against obesity and associated metabolic diseases, including type 2 diabetes. The aim of this study was to compare the effectiveness of a balanced Mediterranean diet with a low-carbohydrate diet on weight loss and glucose homeostasis in morbidly obese individuals at high risk to develop diabetes. Insulin secretion, insulin clearance, and different β-cell function components were estimated by modeling plasma glucose, insulin and C-peptide profiles during 75-g oral glucose tolerance tests (OGTTs) performed at baseline and after 4 weeks of each dietary intervention. The average weight loss was 5%, being 58% greater in the low-carbohydrate-group than Mediterranean-group. Fasting plasma glucose and glucose tolerance were not affected by the diets. The two dietary regimens proved similarly effective in improving insulin resistance and fasting hyperinsulinemia, while enhancing endogenous insulin clearance and β-cell glucose sensitivity. In summary, we demonstrated that a low-carbohydrate diet is a successful short-term approach for weight loss in morbidly obese patients and a feasible alternative to the Mediterranean diet for its glucometabolic benefits, including improvements in insulin resistance, insulin clearance and β-cell function. Further studies are needed to compare the long-term efficacy and safety of the two diets.

Genetic Polymorphisms of β-Cell Differentiation Confer Risk of Alterations of Glucose Metabolism in Survivors of Childhood Acute Lymphoblastic Leukemia.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 1908-1908
Author(s):  
Pacharapan Surapolchai ◽  
Suradej Hongeng ◽  
Pat Mahachoklertwattana ◽  
Samart Pakakasama ◽  
Angkana Winaichatsak ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Cell Function ◽  
Lymphoblastic Leukemia ◽  
Β Cell ◽  
Childhood All ◽  
Β Cell Function

Abstract Purpose: Long-term survivors of acute lymphoblastic leukemia (ALL) seem to be at risk of insulin resistance, impaired glucose tolerance and may develop typical signs of metabolic syndrome with disturbances in lipid metabolism. The aim of the present study was to study the prevalence of alterations in glucose metabolism and the predisposing factors of these disturbances in survivors of childhood ALL. Furthermore, we intended to identify the role of such genetic polymorphisms affecting β-cell function and glucose metabolism and possibly to develop them as markers for monitoring β-cell dysfunction following treatment for ALL in the future. Patients and methods: In 131 ALL survivors after cessation of therapy, an oral glucose tolerance test was performed to determine β-cell function/insulin sensitivity. Six single-nucleotide polymorphisms of PAX4 and TCF7L2 genes were genotyped in order to evaluate the association between these polymorphisms and β-cell function/insulin sensitivity. Results: Ten out of 131 (7.6%) survivors had impaired glucose tolerance (IGT) while 40 out of 131 (30.5%) had insulin resistance (IR) and demonstrated characteristics of metabolic syndrome (hyperinsulinemia, hypertriglyceridemia, low HDL-C). In the logistic regression analysis, the most important factor predicting IGT and IR was older current age (p= 0.010 and <0.001, respectively) while the PAX4 R192H mutation (rs2233580) was significant associated only to IGT after adjusted for age (p=0.043) (adjusted OR 5.28, 95%CI 1.06–26.40). Conclusion: Our findings suggest that older age of childhood ALL survivors is the most important risk factor of IGT and IR, underlining the need to continue regular and long-term screening till adulthood. Moreover, after adjusted for age, the PAX4 R192H variant (rs2233580) seemed to be associated with IGT. If this association is confirmed, institution of lifestyle and therapeutic measures may be needed to reduce metabolic risk and diabetes.

scholarly journals Modeling disease progression in newly diagnosed type 2 diabetes

2020 ◽  
Author(s):  
Kun Hao ◽  
Yanguang Cao
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Glycemic Control ◽  
Disease Progression ◽  
Cell Function ◽  
Early Stage ◽  
Β Cell ◽  
Β Cell Function

ABSTRACTType 2 diabetes (T2DM) is a progressive disease, which is primarily characterized by a decline in β-cell function and worsening of insulin resistance. Unfortunately, most interventions (lifestyle, diet, and therapeutic agents) for T2DM only provide a transient restoration of β-cell function and the progression is inevitable once it starts. To understand the natural progression of T2DM, a mechanistic model was developed to quantitatively characterize the dynamic interactions among β-cell function, plasma fasting glucose (PFG), fasting insulin (FI), and the degree of insulin resistance, starting from an early stage of T2DM over up to 8 years. The model was validated using clinical data to optimize the disease parameters. The restoration and deterioration rates of β-cell function were both predicted as 84.5 %/year and 1.10 /year for early stages of T2DM. The model predicted a positive correlation between the initial level of β-cell function at diagnosis and its maximum restoration potential, underscoring the importance of early diagnosis and intervention. After the treatment, β-cell function could be temporarily restored within several months, which has a long-term benefit in glycemic control. The maximal tolerated PFG level that permits β-cell function restoration was predicted to be around 8.33 nM; and the temporal restoration of β-cell function would be unlikely at a PFG level above this threshold. The intrinsic deterioration rates of β-cell function and insulin resistance were both critical factors for long-term glycemic control. In conclusion, our model provides a quantitative analysis of the natural disease progression in T2DM and yields insights into factors that are critical for long-term glycemic control.

Effects of Ovariectomy on Insulin Resistance and β-Cell Function and Mass

2004 ◽  
Vol 9 (4) ◽  
pp. 367-373
Author(s):  
Soo-Bong Choi ◽  
Chun-Hee Park ◽  
Dong-Wha Jun ◽  
Jin-Sun Jang ◽  
Sun-Min Park
Keyword(s):  
Insulin Resistance ◽  
Cell Function ◽  
Β Cell ◽  
Β Cell Function

scholarly journals Association of serum 25-hydroxyvitamin D with insulin resistance and β-cell function in a healthy Chinese female population

2013 ◽  
Vol 34 (8) ◽  
pp. 1070-1074 ◽  
Author(s):  
Min-fang Tao ◽  
Zeng Zhang ◽  
Yao-hua Ke ◽  
Jin-wei He ◽  
Wen-zhen Fu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Cell Function ◽  
Β Cell ◽  
Female Population ◽  
Hydroxyvitamin D ◽  
Β Cell Function ◽  
25 Hydroxyvitamin D ◽  
Healthy Chinese

scholarly journals Maternal high-fat diet induces insulin resistance and deterioration of pancreatic β-cell function in adult offspring with sex differences in mice

2014 ◽  
Vol 306 (10) ◽  
pp. E1163-E1175 ◽  
Author(s):  
Hisashi Yokomizo ◽  
Toyoshi Inoguchi ◽  
Noriyuki Sonoda ◽  
Yuka Sakaki ◽  
Yasutaka Maeda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Sex Differences ◽  
High Fat Diet ◽  
Cell Function ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Plasma Estradiol ◽  
Β Cell Function ◽  
Estradiol Levels

Intrauterine environment may influence the health of postnatal offspring. There have been many studies on the effects of maternal high-fat diet (HFD) on diabetes and glucose metabolism in offspring. Here, we investigated the effects in male and female offspring. C57/BL6J mice were bred and fed either control diet (CD) or HFD from conception to weaning, and offspring were fed CD or HFD from 6 to 20 wk. At 20 wk, maternal HFD induced glucose intolerance and insulin resistance in offspring. Additionally, liver triacylglycerol content, adipose tissue mass, and inflammation increased in maternal HFD. In contrast, extending previous observations, insulin secretion at glucose tolerance test, islet area, insulin content, and PDX-1 mRNA levels in isolated islets were lower in maternal HFD in males, whereas they were higher in females. Oxidative stress in islets increased in maternal HFD in males, whereas there were no differences in females. Plasma estradiol levels were lower in males than in females and decreased in offspring fed HFD and also decreased by maternal HFD, suggesting that females may be protected from insulin deficiency by inhibiting oxidative stress. In conclusion, maternal HFD induced insulin resistance and deterioration of pancreatic β-cell function, with marked sex differences in adult offspring accompanied by adipose tissue inflammation and liver steatosis. Additionally, our results demonstrate that potential mechanisms underlying sex differences in pancreatic β-cell function may be related partially to increases in oxidative stress in male islets and decreased plasma estradiol levels in males.

scholarly journals Common Risk Factors in Relatives and Spouses of Patients with Type 2 Diabetes in Developing Prediabetes

Healthcare ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 1010
Author(s):  
Wei-Hao Hsu ◽  
Chin-Wei Tseng ◽  
Yu-Ting Huang ◽  
Ching-Chao Liang ◽  
Mei-Yueh Lee ◽  
...  
Keyword(s):  
Risk Factors ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Cell Function ◽  
Diabetic Patients ◽  
Β Cell ◽  
Tyg Index ◽  
Β Cell Function

Prediabetes should be viewed as an increased risk for diabetes and cardiovascular disease. In this study, we investigated its prevalence among the relatives and spouses of patients with type 2 diabetes or risk factors for prediabetes, insulin resistance, and β-cell function. A total of 175 individuals were included and stratified into three groups: controls, and relatives and spouses of type 2 diabetic patients. We compared clinical characteristics consisting of a homeostatic model assessment for insulin resistance (HOMA-IR) and beta cell function (HOMA-β), a quantitative insulin sensitivity check index (QUICKI), and triglyceride glucose (TyG) index. After a multivariable linear regression analysis, the relative group was independently correlated with high fasting glucose, a high TyG index, and low β-cell function; the relatives and spouses were independently associated with a low QUICKI. The relatives and spouses equally had a higher prevalence of prediabetes. These study also indicated that the relatives had multiple factors predicting the development of diabetes mellitus, and that the spouses may share a number of common environmental factors associated with low insulin sensitivity.

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