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Boost insulin sensitivity and improve insulin sensitivity index

Boost insulin sensitivity and improve insulin sensitivity index

The potential for nad interval training to reduce cardiometabolic disease risk. They concluded that Boost insulin sensitivity and improve insulin sensitivity index sensitviity a need for more research on the effects of resveratrol supplementation in humans. Takir, M. However, the role of sex hormones in this pathway is unclear, and thus further methodological studies should be conducted.


7 Things That Boost Insulin Sensitivity or Reverse Insulin Resistance - Dr. Berg

Boost insulin sensitivity and improve insulin sensitivity index -

Reviewed by Danielle Kelvas, MD. Updated by. Science-based and reviewed. Foods to Avoid. Foods to Eat. Metabolic Health. Glucose Table of contents Example H2.

Example H3. While this article itself is not directly about diabetes, we will cover some of the key principles of diabetes, such as sugar, insulin, insulin sensitivity, and how to increase insulin sensitivity What Is Insulin?

This means the cell takes sugar and turns it into glycogen, so it can be stored and used later. In fat cells, insulin promotes storing sugar as fat. In muscle cells, insulin promotes protein synthesis and glycogenesis. In pancreas cells, insulin regulates the secretion of glucagon, which is a hormone that facilitates cells releasing stored sugar into the bloodstream.

Insulin and glucagon are hormones that regulate each other. In brain cells, insulin is involved in appetite regulation. This involves the complex interplay of many metabolic pathways, including: 8 Fat lipid metabolites and the creation of fat lipogenesis.

Protein amino acid metabolites and synthesis. Emerging evidence shows increasing links to the gut microbiome. Get more information about weight loss, glucose monitors, and living a healthier life. References Goran, Michael I. Sugarproof: the hidden dangers of sugar that are putting your child's health at risk and what you can do.

Avery, an imprint of Penguin Random House. Diagnosis and classification of diabetes mellitus. Diabetes care, 32 Suppl 1 Suppl 1 , S62—S In: StatPearls [Internet]. Treasure Island FL : StatPearls Publishing; Jan-. Creative Commons Attribution 4.

Fructose: metabolic, hedonic, and societal parallels with ethanol. Journal of the American Dietetic Association, 9 , — Is Sugar Addictive?. Diabetes 1 July ; 65 7 : — Altered brain response to drinking glucose and fructose in obese adolescents.

Yang, Q. Metabolites as regulators of insulin sensitivity and metabolism. Nat Rev Mol Cell Biol 19, — Imamura, F. Effects of Saturated Fat, Polyunsaturated Fat, Monounsaturated Fat, and Carbohydrate on Glucose-Insulin Homeostasis: A Systematic Review and Meta-analysis of Randomised Controlled Feeding Trials.

PLoS medicine, 13 7 , e The Association Between Artificial Sweeteners and Obesity. Current gastroenterology reports, 19 12 , Biomarkers of insulin sensitivity and insulin resistance: Past, present and future.

Critical reviews in clinical laboratory sciences, 52 4 , — Exercise improves adiposopathy, insulin sensitivity and metabolic syndrome severity independent of intensity. Experimental physiology, 4 , — Insulin resistance Syndrome. Am Fam Physician, 63 6 , - Qian, J. Differential effects of the circadian system and circadian misalignment on insulin sensitivity and insulin secretion in humans.

Reviewed December Prevalence of Prediabetes Among Adults. html Soeters, M. The evolutionary benefit of insulin resistance. Clinical Nutrition, Dec;31 6 Ketogenic Diet.

Kerin, Haley J. Webb, Melanie J. Australian Journal of Psychology 70 2 , Metabolic syndrome and insulin resistance: underlying causes and modification by exercise training. Comprehensive Physiology , 3 1 , 1— Haupt, D. Hyperglycemia and antipsychotic medications.

The Journal of clinical psychiatry, 62 Suppl 27, 15— About the author Dr. View Author Bio. Glucose Latest articles. Insulin Resistance and Prediabetes: Symptoms, Risk Factors, and What You Can Do Leann Poston, MD, MBA, M. Signos How to Improve Impaired Fasting Glucose Caitlin Beale, MS, RDN.

Weight Loss. How Excess Insulin Is Associated with Excess Weight William Dixon, MD. Can Seasonal Allergies Spike Blood Sugar? Danielle Kelvas, MD. Blood Sugar and Your Immune System Leann Poston, MD, MBA, M.

Why Is My Blood Sugar High During or After Exercise? Leann Poston, MD, MBA, M. Non-exercise Activity Thermogenesis NEAT for Weight Loss Caitlin Beale, MS, RDN. Peanut Butter Glycemic Index: Nutrition Facts, Weight Loss, Health Benefits Signos Staff.

Peas Glycemic Index: Nutrition Facts, Weight Loss, Health Benefits Signos Staff. Carrot Glycemic Index: Nutrition Facts, Weight Loss, Health Benefits Signos Staff. Is Feta Cheese Good for You? Nutritional Facts and Risks Mia Barnes.

Wegovy vs. Mounjaro: Differences, Dosage, and Side Effects Rebecca Washuta. Beberashvili, I. Serum uric acid as a clinically useful nutritional marker and predictor of outcome in maintenance hemodialysis patients. Nutrition 31, — Bertoli, A. Differences in insulin receptors between men and menstruating women and influence of sex hormones on insulin binding during the menstrual cycle.

Bird, S. Update on the effects of physical activity on insulin sensitivity in humans. BMJ Open Sport Exerc. CrossRef Full Text Google Scholar.

Bjornstad, P. Pathogenesis of lipid disorders in insulin resistance: a brief review. Borghouts, L. Exercise and insulin sensitivity: a review. Sports Med. Church, T. Exercise in obesity, metabolic syndrome, and diabetes. Cicero, A. Long-term predictors of impaired fasting glucose and type 2 diabetes in subjects with family history of type 2 diabetes: a years follow-up of the Brisighella heart study historical cohort.

Diabetes Res. Curtin, L. National Health and Nutrition Examination Survey: sample design, Vital Health Stat. Davies, K. Uric acid-iron ion complexes. A new aspect of the antioxidant functions of uric acid. Despres, J. Treatment of obesity: need to focus on high risk abdominally obese patients. BMJ , — DiPietro, L.

Exercise and improved insulin sensitivity in older women: evidence of the enduring benefits of higher intensity training. Duncan, G.

Exercise, fitness, and cardiovascular disease risk in type 2 diabetes and the metabolic syndrome. Eriksson, K. Prevention of type 2 non-insulin-dependent diabetes mellitus by diet and physical exercise. The 6-year Malmo feasibility study. Diabetologia 34, — Erlichman, J. Physical activity and its impact on health outcomes.

Paper 1: the impact of physical activity on cardiovascular disease and all-cause mortality: an historical perspective. Festa, A. Nuclear magnetic resonance lipoprotein abnormalities in prediabetic subjects in the insulin resistance atherosclerosis study.

Circulation , — Fraile-Bermudez, A. Relationship between physical activity and markers of oxidative stress in independent community-living elderly individuals. Freeman, A.

Insulin Resistance. Treasure Island FL : StatPearls. Garber, C. American College of Sports, American College of Sports Medicine position stand. Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise.

Gardner, A. Association between daily walking and antioxidant capacity in patients with symptomatic peripheral artery disease. Grundy, S. Small LDL, atherogenic dyslipidemia, and the metabolic syndrome.

Circulation 95, 1—4. Haffner, S. Prospective analysis of the insulin-resistance syndrome syndrome X. Diabetes 41, — Hallal, P.

Lancet physical activity series working, global physical activity levels: surveillance progress, pitfalls, and prospects. Lancet , — Han, T. Temporal relationship between hyperuricemia and insulin resistance and its impact on future risk of hypertension.

Hypertension 70, — He, F. Redox mechanism of reactive oxygen species in exercise. Herzig, K. Light physical activity determined by a motion sensor decreases insulin resistance, improves lipid homeostasis and reduces visceral fat in high-risk subjects: PreDiabEx study RCT.

Howard, B. LDL cholesterol as a strong predictor of coronary heart disease in diabetic individuals with insulin resistance and low LDL: The strong heart study.

Hu, L. U-shaped association of serum uric acid with all-cause and cause-specific mortality in US adults: A cohort study. Hu, F. Adiposity as compared with physical activity in predicting mortality among women. Huttunen, J. Effect of moderate physical exercise on serum lipoproteins. A controlled clinical trial with special reference to serum high-density lipoproteins.

Circulation 60, — Jia, Z. Serum uric acid levels and incidence of impaired fasting glucose and type 2 diabetes mellitus: a meta-analysis of cohort studies.

Kessler, H. The potential for high-intensity interval training to reduce cardiometabolic disease risk. Khosla, U. Hyperuricemia induces endothelial dysfunction. Kidney Int. Krishnan, E. Hyperuricemia in young adults and risk of insulin resistance, prediabetes, and diabetes: a year follow-up study.

Lanaspa, M. Uric acid induces hepatic steatosis by generation of mitochondrial oxidative stress: potential role in fructose-dependent and -independent fatty liver. Lehtonen, A. Serum triglycerides and cholesterol and serum high-density lipoprotein cholesterol in highly physically active men.

Acta Med. Manson, J. Physical activity and incidence of non-insulin-dependent diabetes mellitus in women. Mazidi, M. The link between insulin resistance parameters and serum uric acid is mediated by adiposity. Atherosclerosis , — Medina-Santillan, R.

Hepatic manifestations of metabolic syndrome. Diabetes Metab. Myers, J. Fitness versus physical activity patterns in predicting mortality in men. Nakagawa, T. A causal role for uric acid in fructose-induced metabolic syndrome. Nakamura, K. HOMA-IR and the risk of hyperuricemia: a prospective study in non-diabetic Japanese men.

National Center for Chronic Disease and Health Promotion National Diabetes Statistics Report, Estimates of Diabetes and its Burden in the United States.

Atlanta, GA: Division of Diabetes. Patel, C. A database of human exposomes and phenomes from the US National Health and Nutrition Examination Survey.

Data Pearson, T. AHA guidelines for primary prevention of cardiovascular disease and stroke: update: consensus panel guide to comprehensive risk reduction for adult patients Without coronary or other atherosclerotic vascular diseases. American Heart Association science advisory and coordinating committee.

Pirro, M. Uric acid and bone mineral density in postmenopausal osteoporotic women: the link lies within the fat. Rennie, K. Association of the metabolic syndrome with both vigorous and moderate physical activity.

Roberts, C. Metabolic syndrome and insulin resistance: underlying causes and modification by exercise training.

Rowinski, R. Markers of oxidative stress and erythrocyte antioxidant enzyme activity in older men and women with differing physical activity. Roy, D. Insulin stimulation of glucose uptake in skeletal muscles and adipose tissues in vivo is NO dependent. Ruby, B. Gender differences in substrate utilisation during exercise.

Sampath Kumar, A. Exercise and insulin resistance in type 2 diabetes mellitus: a systematic review and meta-analysis.

Sautin, Y. Cell Physiol. Slentz, C. Inactivity, exercise, and visceral fat. STRRIDE: a randomized, controlled study of exercise intensity and amount. Sparks, J. Selective hepatic insulin resistance, VLDL overproduction, and hypertriglyceridemia. Swain, D. Comparison of cardioprotective benefits of vigorous versus moderate intensity aerobic exercise.

Takir, M. Lowering uric acid with allopurinol improves insulin resistance and systemic inflammation in asymptomatic hyperuricemia.

Ter Maaten, J. Renal handling of urate and sodium during acute physiological hyperinsulinaemia in healthy subjects. Toledo-Arruda, A. Time-course effects of aerobic physical training in the prevention of cigarette smoke-induced COPD.

Tuomilehto, J. Finnish diabetes prevention study, prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. Vandenbroucke, J. Strengthening the reporting of observational studies in epidemiology STROBE : explanation and elaboration.

Epidemiology 18, — von Elm, E. The strengthening the reporting of observational studies in epidemiology STROBE statement: guidelines for reporting observational studies. PLoS Med. Wan, X. Uric acid regulates hepatic steatosis and insulin resistance through the NLRP3 inflammasome-dependent mechanism.

Wisloff, U. High-intensity interval training to maximize cardiac benefits of exercise training? Sport Sci.

World Health Organization World Health Statistics Monitoring Health for the SDGs, Sustainable Development Goals. Geneva: World Health Organization.

Licence: CC BY-NC-SA 3. Zhang, D. Leisure-time physical activity and incident metabolic syndrome: a systematic review and dose-response meta-analysis of cohort studies.

Metabolism 75, 36— Citation: Lin Y, Fan R, Hao Z, Li J, Yang X, Zhang Y and Xia Y The Association Between Physical Activity and Insulin Level Under Different Levels of Lipid Indices and Serum Uric Acid.

Received: 08 November ; Accepted: 06 January ; Published: 02 February Copyright © Lin, Fan, Hao, Li, Yang, Zhang and Xia. This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY.

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Sections Sections. About journal About journal. Article types Author guidelines Editor guidelines Publishing fees Submission checklist Contact editorial office. ORIGINAL RESEARCH article Front. The Association Between Physical Activity and Insulin Level Under Different Levels of Lipid Indices and Serum Uric Acid.

Introduction Insulin resistance IR is defined as an impaired biologic response to glucose disposal and insulin stimulation of target tissues mainly the liver, muscle, and adipose tissue , leading to a compensatory increase in beta-cell insulin production and hyperinsulinemia.

Materials and Methods Study Population The National Health and Nutrition Examination Study NHANES , which is a representative survey of the national population in the United States, was conducted by the Centers for Disease Control and Prevention CDC.

Exposure Variables and Outcomes The physical activity the exposure variable of participants between and was based on the Global Physical Activity Questionnaire GPAQ; Hallal et al. Statistical Analysis All statistical analyses were performed using Empower Stats 2.

Table 1. Basic characters. Table 2. The association between physical activity and insulin. com 3. x PubMed Abstract CrossRef Full Text Google Scholar. c PubMed Abstract CrossRef Full Text Google Scholar.

Keywords: physical activity, insulin, NHANES, SUA, lipids Citation: Lin Y, Fan R, Hao Z, Li J, Yang X, Zhang Y and Xia Y The Association Between Physical Activity and Insulin Level Under Different Levels of Lipid Indices and Serum Uric Acid.

Edited by: Hassane Zouhal , University of Rennes 2 — Upper Brittany, France. Reviewed by: Yingyun Gong , Nanjing Medical University, China Lorenzo Romano , University of Rome Tor Vergata, Italy.

Boosy dietary insupin lifestyle Natural hunger suppressant sensitiivty help prevent insulin resistance. Insulin Managing alcohol intake, a condition in which your cells stop responding properly to insulin, is incredibly common. In fact, the prevalence of insulin resistance is However, certain dietary and lifestyle habits can dramatically improve or help prevent this condition. Insulin is a hormone that your pancreas secretes. Boost insulin sensitivity and improve insulin sensitivity index

Boost insulin sensitivity and improve insulin sensitivity index -

The ability of the pancreas to increase insulin production means that insulin resistance alone won't have any symptoms at first.

Over time, though, insulin resistance tends to get worse, and the pancreatic beta cells that make insulin can wear out. Eventually, the pancreas no longer produces enough insulin to overcome the cells' resistance.

The result is higher blood glucose levels, and ultimately prediabetes or type 2 diabetes. Insulin has other roles in the body besides regulating blood glucose levels, and the effects of insulin resistance are thought to go beyond diabetes.

For example, some research has shown that insulin resistance, independent of diabetes, is associated with heart disease. Scientists are beginning to get a better understanding of how insulin resistance develops.

For starters, several genes have been identified that make a person more or less likely to develop the condition. It's also known that older people are more prone to insulin resistance. Lifestyle can play a role, too. Being sedentary, overweight or obese increases the risk for insulin resistance.

It's not clear, but some researchers theorize that extra fat tissue may cause inflammation, physiological stress or other changes in the cells that contribute to insulin resistance. There may even be some undiscovered factor produced by fat tissue, perhaps a hormone, that signals the body to become insulin resistant.

Doctors don't usually test for insulin resistance as a part of standard diabetes care. In clinical research, however, scientists may look specifically at measures of insulin resistance, often to study potential treatments for insulin resistance or type 2 diabetes.

Because this test is so brief, there's very little danger of counter-regulatory hormones interfering with its results. IV access should be established for insulin injection, blood sampling, and for rapid administration of D50W should severe hypoglycemia occur.

These values reflect the rate of decline of log transformed glucose values. Frequently sampled IV glucose tolerance tests FSIVGTT. This method is less labor intensive than clamp techniques yet still requires as many as 25 blood samples over a 3-hour period, and a computer-assisted mathematical analysis.

Several variations of the FSIVGTT have been published. One recently published study infused 0. The SI was calculated by a computer-based program. Tolbutamide administration can also be used during FSIVGTT to augment endogenous insulin secretion and is particularly useful in women with diabetes.

Continuous infusion of glucose with model assessment CIGMA : Like ITT, CIGMA requires fewer venipunctures and is less laborious than clamp techniques. A constant IV glucose infusion is administered, and samples for glucose and insulin are drawn at 50, 55, and 60 minutes. A mathematical model is then used to calculate SI.

The results are reasonably compatible with clamp techniques; however, few laboratories have used CIGMA for insulin sensitivity testing in diabetic patients and there is no substantive data using the CIGMA technique in women with PCOS.

Oral glucose tolerance test OGTT : OGTT, a mainstay in the diagnosis of impaired glucose tolerance IGT and diabetes mellitus in pregnant and nonpregnant women, may be used to assess insulin sensitivity as well. Because no IV access is needed, OGTT is better suited for assessment of large populations than the other techniques we outlined.

A modified OGTT that uses a or g glucose load and measures glucose and insulin at various intervals over 2 to 4 hours has been used in clinical studies. Like other minimal approaches to diagnosis, OGTT provides information on beta cell secretion and peripheral insulin action, and various mathematical equations have been used to provide an SI value.

Insulin resistance has also been assessed qualitatively if one or more insulin values exceed an upper limit of normal at appropriate intervals. Researchers have compared various methods for assessing insulin sensitivity in type 2 diabetics using the OGTT and found good correlations between AUCinsulin, insulin level at minutes I , and the steady state plasma glucose concentrations derived from a modified ITT.

As mentioned before, the search for uncomplicated and inexpensive quantitative tools to evaluate insulin sensitivity has led to development of fasting state homeostatic assessments. These tests are based on fasting glucose and fasting insulin, and use straightforward mathematical calculations to assess insulin sensitivity and beta cell function.

Several homeostatic approaches have been developed in recent years, each with its merits and deficiencies. One of the weaknesses of these models is that they assume the relationship between glucose and insulin is linear when in fact it's parabolic.

Fasting insulin I0 : Fasting serum insulin is an inexpensive assay, and does not require any mathematical calculations. At least one researcher has advocated averaging two or three readings to account for day-to-day variability.

Although I0 is less variable than other fasting procedures in normoglycemic patients, clinicians must still interpret results cautiously. Remember that insulin sensitivity is the ability of the hormone to reduce serum glucose.

If fasting glucose is high—for example, in a patient with impaired glucose tolerance—that may indicate a diminished effect from circulating insulin or in severe cases of insulin resistance, diminished quantity of the hormone.

Hence I0 should not be used in glucose-intolerant or diabetic patients. Our study included 28 nonobese, 13 obese, and 15 diabetic subjects whose clinical characteristics are listed in Table 2.

Among these subjects were 38 Caucasians, 11 African-Americans, 5 Asians, and 2 Hispanics. Diabetic subjects met the American Diabetes Association criteria for type 2 diabetes Subjects with liver or pulmonary disease as well as end-organ damage, such as renal insufficiency, coronary artery disease, heart failure, peripheral vascular disease, proliferative retinopathy, or diabetic neuropathy, were excluded from our study.

We also obtained an independent dataset from the Division of Endocrinology and Metabolism at Indiana University School of Medicine. This comprised glucose clamp data obtained from 21 obese subjects BMI, Data shown are the mean ± sem from the glucose clamp studies.

At approximately h, after an overnight fast of at least 10 h, subjects were admitted as out-patients to the Clinical Center at NIH and placed in a recumbent position in an adjustable bed.

An iv catheter was placed in an antecubital vein for infusion of insulin, glucose, and potassium phosphate. Another catheter was placed in the contralateral hand for blood sampling. The hand used for sampling was warmed with a heating pad to arterialize the blood.

The insulin solution was allowed to dwell in the iv lines for at least 15 min, and the lines were then flushed before the beginning of the insulin infusion. A solution of potassium phosphate was infused at the same time 0.

Blood glucose concentrations were measured at the bedside every 5—10 min using a glucose analyzer YSI Select, YSI, Inc.

Blood samples were also collected every 20—30 min for determination of plasma insulin concentrations IMX assay, Abbott Laboratories, North Chicago, IL. Intravenous catheters were placed in the antecubital vein of each arm.

An insulin- modified FSIVGTT was performed as described previously Briefly, a bolus of glucose 0. Blood samples were collected for blood glucose and plasma insulin determinations as previously described Data were subjected to minimal model analysis using the computer program MINMOD gift from R.

Bergman to generate predictions of glucose disappearance and insulin sensitivity SI MM We performed a sensitivity analysis of glucose and insulin data from the glucose clamp and the first 20 min of the FSIVGTT of an initial subset of 14 normal, 5 obese, and 3 diabetic subjects to determine the time points that contained the most critical information related to insulin sensitivity as defined by SI Clamp.

We found that changes in fasting insulin and glucose levels were the most related to changes in SI Clamp.

After QUICKI was derived from the initial subset of data, comparisons between QUICKI and the other indexes of insulin sensitivity were performed on the entire set of 28 nonobese, 13 obese, and 15 diabetic subjects. We also calculated QUICKI for the 21 obese and 14 nonobese subjects from Indiana University School of Medicine.

Correlations r between pairs of indexes of insulin sensitivity were calculated. To evaluate the significance of differences in r values for various pairs of indexes, a percentile method bootstrap technique was used to calculate P values The bootstrap was necessary because the r values were based on the same subjects, and thus, pairs of r values are not statistically independent.

Mean BMI, fasting glucose, and fasting insulin values were calculated for each group of subjects Table 2. As expected, the fasting glucose levels for both nonobese and obese groups were normal, whereas the diabetic group had elevated levels.

Steady state conditions were generally achieved about 2 h after the initiation of each study and were maintained for at least 60 min. The mean values for SI Clamp calculated from these data were 6. Hyperinsulinemic isoglycemic glucose clamp studies in 28 nonobese top , 13 obese middle , and 15 diabetic bottom subjects.

To calculate an alternative insulin sensitivity index for each subject based on minimal model analysis, insulin- modified FSIVGTTs were performed Fig. In addition, endogenous insulin secretion 0—20 min in response to the iv glucose bolus in obese subjects was greater than that in nonobese subjects mean insulin peak, ± 34 vs.

When glucose and insulin data from the FSIVGTT were analyzed using the MINMOD program, minimal model predictions of glucose disappearance fit well with the actual glucose disappearance data Fig. The minimal model index of insulin sensitivity SI MM was 5. Note that for 7 of the 15 diabetic subjects, minimal model analysis generated large negative values for SI MM implying that rises in insulin somehow cause glucose levels to increase in these subjects.

This is a well documented artifact of the minimal model that occurs when data from subjects with poor insulin secretion are analyzed Therefore, the minimal model results for these 7 diabetic subjects were excluded from our analyses.

Insulin-modified FSIVGTTs in 28 nonobese top , 13 obese middle , and 15 diabetic bottom subjects. To derive a novel index of insulin sensitivity, we analyzed data obtained from an initial subset of studies in 14 nonobese, 5 obese, and 3 diabetic subjects. We used a sensitivity analysis to determine which data points from the first 20 min of the FSIVGTT contained the most information about insulin sensitivity as determined by SI Clamp.

For nonobese and obese subjects, we discovered that fasting insulin levels correlated well with SI Clamp. Moreover, because fasting insulin levels had a skewed distribution, log transformation of these data was even more highly correlated with SI Clamp.

This result is consistent with the reasoning that fasted nondiabetic subjects are in a steady state in which normal glucose levels are maintained by appropriately adjusting insulin levels to match the degree of insulin sensitivity.

However, this relationship between fasting insulin and SI Clamp is not maintained for diabetic subjects who have fasting hyperglycemia and are unable to appropriately secrete insulin to fully compensate for their insulin resistance.

Interestingly, we found that the product of fasting insulin and glucose yielded an index of insulin sensitivity that was applicable to both diabetic and nondiabetic subjects. To obtain a positive correlation with SI Clamp and transform the data further, we took the reciprocal of this product.

Subsequent to our initial sensitivity analysis of the first subset of subjects, as described above, QUICKI was calculated for all study subjects mean, 0.

We first compared our glucose clamp-derived estimates of insulin sensitivity with those obtained from minimal model analysis Fig. The overall correlation coefficient r calculated from a linear least squares regression was 0.

In addition, linear regression analysis for the subgroups showed regression lines that were parallel to the overall regression line but shifted up for the nonobese subgroup and shifted down for the obese and diabetic subgroups. However, the parallel relationship between regression lines may not be significant because of the large variability observed in the nonobese group.

As expected, correlations between our glucose clamp and FSIVGTT studies gave results comparable to those of previously published studies c.

Table 1. Correlation between glucose clamp and minimal model indexes of insulin sensitivity. SI Clamp and SI MM were determined as described in Subjects and Methods.

Note that nonsensical values for SI MM were obtained in 7 of 15 diabetic subjects; thus, their results were excluded from this analysis. Linear regression lines are also shown for the subgroup analysis.

We next compared our novel index, QUICKI, with SI Clamp Fig. Note that in contrast to the minimal model-derived SI MM , we were able to calculate meaningful values of QUICKI for all diabetic subjects studied.

However, we could only calculate the P value for the differences between these two correlations for the 49 subjects for whom we had complete information on all three methods. We also assessed the interassay reproducibility of QUICKI by comparing SI Clamp to QUICKI derived from baseline blood samples obtained during the FSIVGTT performed at least 1 week apart from the glucose clamp.

The linear regression lines for the subgroup analysis followed the overall regression more closely than when SI Clamp was compared with SI MM.

To validate QUICKI with a completely independent dataset, we also correlated QUICKI with SI Clamp using data from Indiana University School of Medicine.

Interestingly, among these nonobese subjects, one individual had an extremely low BMI of Correlation between SI Clamp and QUICKI. QUICKI was calculated from fasting glucose and insulin values obtained from glucose clamp studies. However, linear regression analysis for the subgroups revealed that the regression line for the diabetic and obese subgroups had a very different slope than that for the nonobese group.

As HOMA becomes larger with decreased insulin sensitivity, we compared SI Clamp with HOMA to obtain a positive correlation Fig. Strikingly, linear regression analysis of the subgroups showed that the nonobese group had a regression line with a very steep slope, whereas the obese group had a more moderate slope, and the diabetic group had a very shallow slope.

These results suggest that HOMA does not vary linearly across wide ranges of insulin sensitivity and patient groups. Correlation between SI MM and QUICKI. Correlation between SI Clamp and HOMA.

HOMA was calculated from fasting glucose and insulin values obtained from glucose clamp studies. Overall correlation coefficients r between various indexes of insulin sensitivity derived from our data obtained during glucose clamp and FSIVGTT studies.

SI Clamp , SI MM , and QUICKI were calculated as described in Materials and Methods. Because HOMA is negatively correlated with insulin sensitivity, the sign of HOMA was reversed when calculating correlation coefficients between HOMA and SI Clamp or QUICKI.

We performed both hyperinsulinemic isoglycemic glucose clamps and insulin-modified FSIVGTTs in nonobese, obese, and diabetic subjects with a wide range of insulin sensitivities. As expected, when subjects were evaluated with the gold standard glucose clamp method, obese subjects were more insulin resistant, on the average, than nonobese subjects, and diabetics were the most insulin-resistant group.

In contrast, when the same subjects underwent FSIVGTT and minimal model analysis, the obese group seemed to have the greatest level of insulin resistance. This is most likely due to the fact that 7 of 15 diabetic subjects had to be excluded from analysis because the minimal model was unable to identify meaningful estimates of insulin sensitivity in these cases.

Indeed, these 7 excluded subjects had higher levels of insulin resistance than the other diabetic subjects as assessed by glucose clamp. The inability of the minimal model to identify meaningful values for SI MM in a large fraction of our diabetic subjects is consistent with the experience of others and is most likely related to well described difficulties in estimating SI MM under conditions of inadequate insulin secretion The overall correlation we obtained between SI Clamp and SI MM was comparable to previous reports whose study subjects included diabetics, suggesting that our studies were technically adequate.

Nevertheless, the level of correlation obtained between direct measures of insulin sensitivity i. glucose clamp and indirect measures, such as minimal model analysis, in both the present study and previous studies suggests that investigators should be cautious in applying minimal model analysis of insulin sensitivity to population studies.

This is further highlighted by recent studies demonstrating particular inadequacies of the minimal model approach that result in overestimation of glucose effectiveness and underestimation of insulin sensitivity 14, Although the glucose clamp is considered to be the gold standard method for directly measuring insulin sensitivity in vivo, it can be implemented in a number of different ways.

That is, achieving a high steady state insulin level in these subjects may be required to measure a significant effect of insulin on net glucose disposal.

The good correlation we obtained between studies performed at low and high insulin infusion rates suggests that the higher insulin infusion rate was also appropriate for the nonobese subjects.

We decided to clamp glucose levels at the fasting value isoglycemic clamp rather than at normal levels euglycemic clamp because acute changes in insulin sensitivity related to large changes in glycemia may complicate the interpretation of glucose clamp results.

In the case of nonobese and obese subjects who had normal fasting glucose levels, the isoglycemic clamp is equivalent to a euglycemic clamp. Diabetic subjects were taken off of antidiabetic medication for 1 week before each study, and the glucose clamp was performed under isoglycemic conditions to avoid difficulties in interpretation of glucose clamp data that are acquired at levels of glycemia acutely different from fasting levels.

We only explored the first 20 min of the FSIVGTT data because the insulin infusion initiated at 20 min would necessitate the development of a test complicated by iv infusion of insulin. After the QUICKI formula was derived from the initial subset of subjects, we then analyzed our entire study population.

Similar to our results from glucose clamp studies and in contrast to minimal model results , insulin sensitivity as assessed by QUICKI was highest in the nonobese group, intermediate in the obese group, and lowest in the diabetic group. More importantly, the overall correlation between QUICKI and SI Clamp was significantly better than that obtained between SI MM and SI Clamp.

In addition, the linear regression analysis of the subgroups corresponded more closely to the overall regression line when comparing QUICKI and SI Clamp. Taken together with the fact that the overall correlation between QUICKI and SI Clamp was also better than the correlation between QUICKI and SI MM , our results suggest that QUICKI contains additional independent information about insulin sensitivity that is not captured by the minimal model approach.

Furthermore, QUICKI provides a reproducible and robust estimate of insulin sensitivity, because equally strong correlations with SI Clamp were obtained when fasting data from either the glucose clamp or FSIVGTT studies were used to calculate QUICKI.

In addition, QUICKI derived from the average results of two fasting blood samples over 10 min was similar to QUICKI calculated from a single sample.

Finally, the good correlation between QUICKI and SI Clamp obtained from a completely independent dataset acquired at a different institution provides further validation of the reliability of QUICKI.

However, the correlation coefficient for the nonobese subgroup was 0. There are several potential explanations for the lower correlation we observed within the nonobese subgroup.

The most likely explanation for this finding is that variability in insulin determinations due to limitations in assay sensitivity causes larger percentage of errors in QUICKI when insulin levels are lowest typical of the most insulin-sensitive subjects.

Alternatively, periodic oscillations in insulin secretion both ultradian and to min periods have been reported in healthy subjects and may also contribute to the weaker correlation in this subgroup 21 , Interestingly, these oscillations diminish with impaired glucose tolerance and diabetes 23 , Therefore, in our nonobese subjects there may be a sampling error that results in aliasing of the data.

However, this effect is unlikely to be occurring in our studies, because fasting samples were obtained at the same time in the morning for each subject, and calculating QUICKI from the average of several blood samples instead of a single sample did not significantly affect our correlations.

Another possible explanation for the lower correlation between QUICKI and SI Clamp in the nonobese subgroup is that the insulin infusion rate used in our glucose clamp studies was inappropriately high for individuals who are very insulin sensitive.

Nevertheless, as discussed above, the good correlation between SI Clamp derived from high and low insulin infusion rates suggests that our choice of high insulin infusion rate did not introduce significant error into SI Clamp estimates in nonobese subjects.

However, it is possible that comparison of QUICKI with clamp data obtained with low insulin infusion rates has additional variability, because hepatic glucose production may not be completely suppressed under these conditions. Previous studies have suggested that fasting insulin per se may provide a reasonable index of insulin sensitivity that has positive predictive power with respect to the development of diseases associated with insulin resistance, such as obesity, hypertension, and diabetes 25 — However, in diabetes, where fasting hyperglycemia is accompanied by inadequate insulin secretion, this relationship may not be maintained.

To account for this, the so-called HOMA approach uses a mathematical model to obtain an insulin sensitivity index that is defined as the product of the fasting plasma insulin and blood glucose values divided by a constant

Seneitivity changes sensiticity the body begin long Boost insulin sensitivity and improve insulin sensitivity index a person is diagnosed with type 2 diabetes. One of the most important unseen changes? Insulin resistance. Insulin is a key player in developing type 2 diabetes. Here are the high points:.

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  1. Nach meiner Meinung sind Sie nicht recht. Es ich kann beweisen. Schreiben Sie mir in PM, wir werden umgehen.

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