Effect of prior moderate exercise on postprandial metabolism in men with type 2 diabetes: Heterogeneity of responses

2007 ◽  
Vol 194 (1) ◽  
pp. 134-143 ◽  
Author(s):  
Jason M.R. Gill ◽  
Ali Al-Mamari ◽  
William R. Ferrell ◽  
Stephen J. Cleland ◽  
Colin G. Perry ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Moderate Exercise ◽  
Postprandial Metabolism

The Scientific Case against Prescribing Insulin for Treatment of Type 2 Diabetes

2021 ◽  
pp. 1-3
Author(s):  
John F Burd
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Clinical Studies ◽  
Nutritional Supplement ◽  
The United States ◽  
Intermittent Fasting ◽  
Moderate Exercise ◽  
Double Blind ◽  
Double Blind Placebo

Obesity and type 2 diabetes are related worldwide epidemics which could be erased with the help of governments and medical communities using tools that are readily available today. Prevailing diet recommendations, which are clearly wrong, are a significant cause of both obesity and type 2 diabetes and have led to the current dire situation. According to the CDC, in the United States alone there are currently 34.2 million people with diabetes of which 30 million have type 2 diabetes. In addition, 88 million Americans have prediabetes (defined as an A1c above 5.7%) which will almost certainly progress to type 2 diabetes if not treated and reversed. The cause of insulin resistance, prediabetes and type 2 diabetes is “glucose toxicity” as explained below, and understanding this medical term is paramount to the case against using insulin for type 2 diabetes. Glucose reacts with all the proteins in the body leading to insulin resistance and type 2 diabetes. Unfortunately, nearly 20% of adults with type 2 diabetes are prescribed insulin injections often in conjunction with oral pharmaceutical medications. Because people with with type 2 diabetes have insulin resistance, prescribing insulin is a very bad idea, since they will need an ever-increasing dosage of insulin as time passes, leading to a lifetime of insulin injections. There is only one product, Lysulin (www.lysulin.com), that targets the cause of insulin resistance and has been proven in double blind, placebo controlled clinical studies to improve insulin resistance and better cell function. The recommend initial treatment for type 2 diabetes should be moderate exercise, intermittent fasting, a low calorie, low carbohydrate ketrogenic diet combined with Lysulin before instituting insulin therapy for type 2 diabetes. By adhering to a ketogenic diet that includes moderate exercise, intermittent fasting and nutritional supplementation with Lysulin, diabetes can be halted and quite possibly reversed. Lysulin is a patented nutritional supplement that contains lysine, zinc, and vitamin C [1]. Double-blind placebo-controlled clinical studies have shown the effectiveness of this nutritional supplement [2, 3].

scholarly journals Impact of metformin versus the prandial insulin secretagogue, repaglinide, on fasting and postprandial glucose and lipid responses in non-obese patients with type 2 diabetes

2008 ◽  
Vol 158 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Søren S Lund ◽  
Lise Tarnow ◽  
Merete Frandsen ◽  
Ulla M Smidt ◽  
Oluf Pedersen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Ldl Cholesterol ◽  
Density Lipoprotein ◽  
Postprandial Glucose ◽  
Obese Patients ◽  
Postprandial Metabolism ◽  
Insulin Secretagogue ◽  
Prandial Insulin ◽  
Glucose And Lipid Metabolism

ObjectiveNon-obese patients with type 2 diabetes (T2DM) are characterized by predominant defective insulin secretion. However, in non-obese T2DM patients, metformin, targeting insulin resistance, is non-inferior to the prandial insulin secretagogue, repaglinide, controlling overall glycaemia (HbA1c). Whether the same apply for postprandial glucose and lipid metabolism is unknown. Here, we compared the effect of metformin versus repaglinide on postprandial metabolism in non-obese T2DM patients.DesignSingle-centre, double-masked, double-dummy, crossover study during 2×4 months involving 96 non-obese (body mass index≤27 kg/m2) insulin-naïve T2DM patients. At enrolment, patients stopped prior oral hypoglycaemic agents therapies and after a 1-month run-in period on diet-only treatment, patients were randomized to repaglinide (2 mg) thrice daily followed by metformin (1 g) twice daily or vice versa each during 4 months with 1-month washout between interventions.MethodsPostprandial metabolism was evaluated by a standard test meal (3515 kJ; 54% fat, 13% protein and 33% carbohydrate) with blood sampling 0–6 h postprandially.ResultsFasting levels and total area under the curve (AUC) for plasma glucose, triglycerides and free fatty acids (FFA) changed equally between treatments. In contrast, fasting levels and AUC of total cholesterol, low-density lipoprotein (LDL) cholesterol, non-high-density lipoprotein (non-HDL) cholesterol and serum insulin were lower during metformin than repaglinide (mean (95% confidence intervals), LDL cholesterol difference metformin versus repaglinide: AUC: −0.17 mmol/l (−0.26; −0.08)). AUC differences remained significant after adjusting for fasting levels.ConclusionsIn non-obese T2DM patients, metformin reduced postprandial levels of glycaemia, triglycerides and FFA similarly compared to the prandial insulin secretagogue, repaglinide. Furthermore, metformin reduced fasting and postprandial cholesterolaemia and insulinaemia compared with repaglinide. These data support prescription of metformin as the preferred drug in non-obese patients with T2DM targeting fasting and postprandial glucose and lipid metabolism.

Frequency of Interruptions to Sitting Time: Benefits for Postprandial Metabolism in Type 2 Diabetes

Diabetes Care ◽  
2021 ◽  
pp. dc201410
Author(s):  
Ashleigh R. Homer ◽  
Frances C. Taylor ◽  
Paddy C. Dempsey ◽  
Michael J. Wheeler ◽  
Parneet Sethi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Sitting Time ◽  
Postprandial Metabolism

Exercise excess pressure and exercise-induced albuminuria in patients with type 2 diabetes mellitus

2015 ◽  
Vol 308 (9) ◽  
pp. H1136-H1142 ◽  
Author(s):  
Rachel E. D. Climie ◽  
Velandai Srikanth ◽  
Laura J. Keith ◽  
Justin E. Davies ◽  
James E. Sharman
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Aortic Stiffness ◽  
Significant Rise ◽  
Excess Pressure ◽  
Moderate Exercise ◽  
Central Hemodynamics ◽  
Exercise Induced

Exercise-induced albuminuria is common in patients with type 2 diabetes mellitus (T2DM) in response to maximal exercise, but the response to light-moderate exercise is unclear. Patients with T2DM have abnormal central hemodynamics and greater propensity for exercise hypertension. This study sought to determine the relationship between light-moderate exercise central hemodynamics (including aortic reservoir and excess pressure) and exercise-induced albuminuria. Thirty-nine T2DM (62 ± 9 yr; 49% male) and 39 nondiabetic controls (53 ± 9 yr; 51% male) were examined at rest and during 20 min of light-moderate cycle exercise (30 W; 50 revolutions/min). Albuminuria was assessed by the albumin-creatinine ratio (ACR) at rest and 30 min postexercise. Hemodynamics recorded included brachial and central blood pressure (BP), aortic stiffness, augmented pressure (AP), aortic reservoir pressure, and excess pressure integral (Pexcess). There was no difference in ACR between groups before exercise ( P > 0.05). Exercise induced a significant rise in ACR in T2DM but not controls (1.73 ± 1.43 vs. 0.53 ± 1.0 mg/mol, P = 0.002). All central hemodynamic variables were significantly higher during exercise in T2DM (i.e., Pexcess, systolic BP and AP; P < 0.01 all). In T2DM (but not controls), exercise Pexcess was associated with postexercise ACR ( r = 0.51, P = 0.002), and this relationship was independent of age, sex, body mass index, heart rate, aortic stiffness, antihypertensive medication, and ambulatory daytime systolic BP (β = 0.003, P = 0.003). Light-moderate exercise induced a significant rise in ACR in T2DM, and this was independently associated with Pexcess, a potential marker of vascular dysfunction. These novel findings suggest that Pexcess could be important for appropriate renal function in T2DM.

scholarly journals Incretin Hormones and Type 2 Diabetes—Mechanistic Insights and Therapeutic Approaches

Biology ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 473
Author(s):  
Geke Aline Boer ◽  
Jens Juul Holst
Keyword(s):  
Type 2 Diabetes ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Incretin Hormones ◽  
Postprandial Metabolism ◽  
Dipeptidyl Peptidase 4 ◽  
Receptor Agonists ◽  
Control Of Diabetes ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are secreted from the gut upon nutrient stimulation and regulate postprandial metabolism. These hormones are known as classical incretin hormones and are responsible for a major part of postprandial insulin release. The incretin effect is severely reduced in patients with type 2 diabetes, but it was discovered that administration of GLP-1 agonists was capable of normalizing glucose control in these patients. Over the last decades, much research has been focused on the development of incretin-based therapies for type 2 diabetes. These therapies include incretin receptor agonists and inhibitors of the incretin-degrading enzyme dipeptidyl peptidase-4. Especially the development of diverse GLP-1 receptor agonists has shown immense success, whereas studies of GIP monotherapy in patients with type 2 diabetes have consistently been disappointing. Interestingly, both GIP-GLP-1 co-agonists and GIP receptor antagonists administered in combination with GLP-1R agonists appear to be efficient with respect to both weight loss and control of diabetes, although the molecular mechanisms behind these effects remain unknown. This review describes our current knowledge of the two incretin hormones and the development of incretin-based therapies for treatment of type 2 diabetes.

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