Association between daily number of eating occasions with fasting glucose and insulin sensitivity in adults from families at high risk for type 2 diabetes in Europe: the Feel4Diabetes Study

Nutrition ◽  
2021 ◽  
pp. 111566
Author(s):  
Kyriaki Apergi ◽  
Kalliopi Karatzi ◽  
Kyriakos Reppas ◽  
Christina Mavrogianni ◽  
Samiah Shadid ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
High Risk ◽  
Fasting Glucose ◽  
Daily Number ◽  
Eating Occasions

Increasing endogenous PPARγ ligands improves insulin sensitivity and protects against diet-induced obesity without side effects of thiazolidinediones

2021 ◽  
Author(s):  
Yu-Hua Tseng ◽  
Lee-Ming Chuang ◽  
Yi-Cheng Chang ◽  
Meng-Lun Hsieh ◽  
Lun Tsou ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Side Effects ◽  
Knockout Mice ◽  
Fasting Glucose ◽  
Binding Mode ◽  
Fluid Retention ◽  
Diet Induced Obesity

Abstract Insulin resistance and obesity are pivotal features of type 2 diabetes mellitus. Peroxisome proliferator-activated receptor γ (PPARγ) is a master transcriptional regulator of systemic insulin sensitivity and energy balance. The anti-diabetic drug thiazolidinediones are potent synthetic PPARγ ligands and insulin sensitizers with undesirable side effects including increased adiposity, fluid retention, and osteoporosis, which limit their clinical use. We and others have proved that 15-keto-PGE2 is an endogenous natural PPARγ ligand. 15-keto-PGE2 is catalyzed by prostaglandin reductase 2 (PTGR2) to become inactive metabolites. We found that 15-keto-PGE2 level is increased in Ptgr2 knockout mice. Ptgr2 knockout mice were protected from diet-induced obesity, insulin resistance, and hepatic steatosis without fluid retention nor reduced bone mineral density. Diet-induced obese mice have drastically reduced 15-keto-PGE2 levels compared to lean mice. Administration of 15-keto-PGE2 markedly improved insulin sensitivity and prevented diet-induced obesity in mice. We demonstrated that 15-keto-PGE2 activates PPARγ through covalent binding to its cysteine 285 residue at helix 3, which restrained its binding pocket between helix 3 and β-sheets of the PPARγ ligand binding domain. This binding mode differs from the helix12-dependent binding mode of thiazolidinediones. We further identified a small-molecule PTGR2 inhibitor BPRPT245, which interferes the interaction between the substrate-binding sites of PTGR2 and 15-keto-PGE2. BPRPT245 increased 15-keto-PGE2 concentration, activated PPARγ, and promoted glucose uptake in adipocytes. BPRPT245 also prevented diet-induced obesity, improved insulin sensitivity and glucose tolerance, lowers fasting glucose without fluid retention and osteoporosis. In humans, reduced serum 15-keto-PGE2 levels were observed in patients with type 2 diabetes compared with controls. Furthermore, serum 15-keto-PGE2 levels correlate inversely with insulin resistance and fasting glucose in non-diabetic humans. In conclusion, we identified a new therapeutic approach to improve insulin sensitivity and protect diet-induced obesity through increasing endogenous natural PPARγ ligands without side effects of thiazolidinediones.

Coffee consumption and type 2 diabetes — An extensive review

Open Medicine ◽  
2008 ◽  
Vol 3 (1) ◽  
pp. 9-19 ◽  
Author(s):  
Siamak Bidel ◽  
Gang Hu ◽  
Jaakko Tuomilehto
Keyword(s):  
Type 2 Diabetes ◽  
Clinical Trials ◽  
Insulin Sensitivity ◽  
Fasting Glucose ◽  
Complex Mixture ◽  
Coffee Consumption ◽  
Epidemiological Studies ◽  
Extensive Review

AbstractCoffee is a complex mixture of potentially active chemicals. It contains significant amounts of phenolic polymers, chlorogenic acid and also caffeine. Agricultural factors, roasting, blending, and brewing determine coffee’s chemical composition. Recent epidemiological studies suggest that habitual coffee consumption may help to prevent some chronic diseases including type 2 diabetes. Despite reports from the clinical trials of the effect of caffeine on decreasing insulin sensitivity, long-term prospective studies revealed that coffee may improve fasting glucose, glucose tolerance and insulin sensitivity as well. In the most recent publication habitual coffee drinkers have a lower total and cardiovascular mortality rate among diabetic subjects.

Hypoglycaemic effect of catalpol in a mouse model of high-fat diet-induced prediabetes

2020 ◽  
Vol 45 (10) ◽  
pp. 1127-1137 ◽  
Author(s):  
Dengqiu Xu ◽  
Xiaofei Huang ◽  
Hozeifa M. Hassan ◽  
Lu Wang ◽  
Sijia Li ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Skeletal Muscle ◽  
Type 2 Diabetes Mellitus ◽  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Mouse Model ◽  
Fasting Glucose ◽  
Hypoglycaemic Effect

Type 2 diabetes mellitus is a major health problem and a societal burden. Individuals with prediabetes are at increased risk of type 2 diabetes mellitus. Catalpol, an iridoid glycoside, has been reported to exert a hypoglycaemic effect in db/db mice, but its effect on the progression of prediabetes is unclear. In this study, we established a mouse model of prediabetes and examined the hypoglycaemic effect, and the mechanism of any such effect, of catalpol. Catalpol (200 mg/(kg·day)) had no effect on glucose tolerance or the serum lipid level in a mouse model of impaired glucose tolerance-stage prediabetes. However, catalpol (200 mg/(kg·day)) increased insulin sensitivity and decreased the fasting glucose level in a mouse model of impaired fasting glucose/impaired glucose tolerance-stage prediabetes. Moreover, catalpol increased the mitochondrial membrane potential (1.52-fold) and adenosine triphosphate content (1.87-fold) in skeletal muscle and improved skeletal muscle function. These effects were mediated by activation of the insulin receptor-1/glucose transporter type 4 (IRS-1/GLUT4) signalling pathway in skeletal muscle. Our findings will facilitate the development of a novel approach to suppressing the progression of diabetes at an early stage. Novelty Catalpol prevents the progression of prediabetes in a mouse model of prediabetes. Catalpol improves insulin sensitivity in skeletal muscle. The effects of catalpol are mediated by activation of the IRS-1/GLUT4 signalling pathway.

scholarly journals Study of Circulating Prohepcidin in Association with Insulin Sensitivity and Changing Iron Stores

2009 ◽  
Vol 94 (3) ◽  
pp. 982-988 ◽  
Author(s):  
José Manuel Fernández-Real ◽  
Francesco Equitani ◽  
José María Moreno ◽  
Melania Manco ◽  
Francisco Ortega ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Iron Metabolism ◽  
Fasting Glucose ◽  
Gene Mutations ◽  
Hfe Gene ◽  
Iron Depletion ◽  
Iron Stores ◽  
Hfe Gene Mutations

Abstract Background: Liver synthesizes hepcidin in response to iron overload, leading to down-regulation of duodenal iron absorption. The pathophysiology of type 2 diabetes is associated with increased iron stores. We aimed to study circulating prohepcidin in association with insulin sensitivity and parameters of glucose and iron metabolism. Methods: Serum prohepcidin was evaluated in three cohorts: 1) a cross-sectional study (cohort 1, men from the general population; n = 135); 2) after decreasing iron stores in men with “high-ferritin” type 2 diabetes (cohort 2; n = 13); and 3) after decreasing iron stores in men carrying HFE gene mutations (cohort 3; n = 16). Insulin sensitivity was measured using either the minimal model or the clamp technique. Results: Circulating prohepcidin correlated significantly with glycated hemoglobin (P < 0.0001), fasting glucose (P = 0.002), triglycerides (P = 0.007), high-density lipoprotein-cholesterol (P = 0.01), ferritin (P = 0.01), and soluble transferrin receptor concentration (P = 0.001) in subjects from cohort 1. Prohepcidin decreased significantly after iron depletion in patients with type 2 diabetes (P = 0.04) (cohort 2) and in carriers of HFE gene mutations (P = 0.03) (cohort 3). In the latter subjects, the change in serum prohepcidin after iron depletion was associated with the change in both fasting glucose transferrin (r = 0.58; P = 0.02) and saturation (r = 0.68; P = 0.005). The changes in insulin sensitivity were associated with those of liver iron content (r = −0.64; P = 0.007) and with those of serum prohepcidin (r = −0.50; P = 0.04) (cohort 3). Conclusions: These associations suggest that circulating prohepcidin concentration is pathophysiologically associated with parameters of glucose and iron metabolism. A failure to increase prohepcidin synthesis is hypothesized to contribute to iron-induced disorders of glucose metabolism.

scholarly journals Type 2 Diabetes Mellitus remission eighteen months after Roux-en-Y gastric bypass.

2016 ◽  
Vol 43 (3) ◽  
pp. 149-153
Author(s):  
MARCELO GOMES GIRUNDI
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Type 2 Diabetes Mellitus ◽  
High Risk ◽  
Glycemic Control ◽  
Fasting Glucose ◽  
Diabetic Patients ◽  
Control Analysis

ABSTRACT Objective: to evaluate the effectiveness of Roux-en-Y gastric bypass in improving the glycemic profile of obese patients with type 2 Diabetes Mellitus (DM2) after 18 months of follow-up. Methods: four hundred sixty-eight pacients with DM2 and BMI ≥35 were submitted to Roux-en-Y gastric bypass, from 1998 to 2010. All patients were submitted to glycemic control analysis in the 3rd, 6th, 9th, 12th and 18th postoperative months. We considered: type 2 diabetic patients, the ones with fasting glucose ≥126mg/dl and HbA1C ≥6.5 in two dosages; high risk patients for diabetes, those who presented fasting glucose ≥ 100 to 125 mg/dl and HbA1C between 5.7%-6.4%; and normal patients, those presenting glucose <100mg/dl and HbA1C <5.7%. Such diagnostic criteria were based on the official position of Sociedade Brasileira de Diabetes, published in July, 2011. Results: The remission of DM2 was seen in 410 (87.6%) out of 468 patients 18 months after the surgery, that being a meaningful difference, with p<0.001. Fourty-eight (10.3%) patients sustained criteria for the disease and ten (2.1%) continued at high risk for DM2. Conclusions: Roux-en-Y gastric bypass was effective in the promotion and maintaince of long-term glycemic control. There are evidences showing that the remission of DM2 is not only related to weight loss and that other enteroinsular axis mechanisms must be involved.

scholarly journals Dietary Behaviors and Glucose Metabolism in Young Adults at Risk for Type 2 Diabetes

2018 ◽  
Vol 44 (2) ◽  
pp. 158-167 ◽  
Author(s):  
EunSeok Cha ◽  
Sudeshna Paul ◽  
Betty J. Braxter ◽  
Guillermo Umpierrez ◽  
Melissa Spezia Faulkner
Keyword(s):  
Type 2 Diabetes ◽  
Young Adults ◽  
Insulin Sensitivity ◽  
High Risk ◽  
African Americans ◽  
Glucose Metabolism ◽  
Beta Cell Function ◽  
Cell Function ◽  
Dietary Behaviors

Purpose The purpose of the study was to examine the associations between dietary behaviors and glucose metabolism in high-risk young adults to increase the precision of nutrition education to prevent early onset type 2 diabetes (T2D). Method Using a descriptive, cross-sectional study design, 106 overweight or obese sedentary young adults ages 18-29 years from the Atlanta metropolitan area were recruited to screen diabetes risk. Survey questionnaires, anthropometric assessment, blood pressure (BP), and laboratory data were collected in a clinical research unit. The Web-based HOMA2 calculator was used to calculate beta cell function and insulin sensitivity. Results The final sample included 103 participants. There were similar patterns of diet (caloric intake and dietary quality) between African Americans and non-African Americans, whereas African Americans showed hyperinsulinemia compared with non-African Americans. When young adults consumed a good quality diet (appropriate carbohydrate intakes; high fiber, low saturated fat but protein rich diet), their insulin resistance was decreased. There was a marginal interaction effect between insulin sensitivity and beta cell function by race. Systolic BP was higher in African Americans, and total cholesterol, triglycerides, and low-density lipoprotein cholesterol were higher in non-African Americans. Conclusion Findings are useful to develop age-specific nutrition guidelines to prevent early onset T2D in high-risk young adults.

scholarly journals Risk perception and unrecognized type 2 diabetes in women with previous gestational diabetes mellitus

2009 ◽  
Vol 2 (3) ◽  
pp. 107-110 ◽  
Author(s):  
Janine Malcolm ◽  
Margaret L Lawson ◽  
Isabelle Gaboury ◽  
Erin Keely
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Risk Perception ◽  
High Risk ◽  
Gestational Diabetes ◽  
Glucose Tolerance ◽  
Fasting Glucose ◽  
Newly Diagnosed ◽  
History Of

Women with a history of gestational diabetes mellitus (GDM) have a high chance of developing type 2 diabetes mellitus (T2DM) following the index pregnancy, however, little is known of women's perception of this risk. The objectives were to (1) determine women's perception of risk of future development of T2DM following a GDM pregnancy and (2) describe the prevalence of undetected dysglycaemia in a Canadian population. The study was designed as a 9–11 year follow-up study of women previously enrolled in a randomized controlled trial of tight versus minimal intervention for GDM. Women's perception of future risk of diabetes was determined by questionnaire. Fasting lipid profile, height and weight were performed on all participants. Oral glucose tolerance tests were performed on all women without prior history of diabetes mellitus type 2 (DM2). The study was conducted at Ottawa Hospital General Campus and Children's Hospital of Eastern Ontario, in Ottawa, Canada. Eighty-nine of 299 (30%) of the original cohort were recruited. Eighty-eight women completed the questionnaire and 77 women without known diabetes underwent two hour glucose tolerance testing. Twenty-three (30%) felt their risk was no different than other women or did not know, 27 (35%) felt risk was increased a little and 27 (35%) felt risk was increased a lot. Only 52% (40/77) had normal glucose tolerance. Of all, 25/88 (28%) patients had diabetes (11 previously diagnosed and 14 diagnosed within the study). Of those newly diagnosed with DM2, four (29%) were diagnosed by fasting glucose, six (42%) by two hour glucose tolerance test (GTT) alone and four (29%) by both. Twenty-four of the women (27%) had impaired glucose tolerance (IGT). Of those with IGT, 12 (57%) had a fasting food glucose < 5.6 mmol/L. In the high-risk perception group with newly diagnosed diabetes, two were overweight, seven were obese, four had a family history of DM2, and all had a waist circumference >88 cm. In conclusion the perception of being at high risk for T2DM did not prevent women from having undetected T2DM. Many factors are likely to contribute to this, including the reliance on screening tests (i.e. fasting glucose) rather than a two hour GTT to detect diabetes. Further studies on effective public and health-care provider education and intervention are needed to identify this high-risk population.

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