Adding fat calories to meals after exercise does not alter glucose tolerance

2004 ◽  
Vol 97 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Amanda K. Fox ◽  
Amy E. Kaufman ◽  
Jeffrey F. Horowitz
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Muscle Glycogen ◽  
Composite Index ◽  
Tolerance Test ◽  
Peak Oxygen Uptake ◽  
Oral Glucose ◽  
High Fat ◽  
Low Fat ◽  
The Hours

A single session of exercise increases insulin sensitivity for hours and even days, and dietary carbohydrate ingested after exercise alters the magnitude and duration of this effect. Although increasing systemic fatty acid availability is associated with insulin resistance, it is uncertain whether increasing dietary fat availability after exercise alters the exercise-induced increase in insulin sensitivity. The purpose of this study was to determine whether adding fat calories to meals after exercise alters glucose tolerance the next day. Seven healthy men cycled 90 min at 66 ± 2% peak oxygen uptake followed by a maximum of five high-intensity intervals. During the hours after exercise, subjects ingested three meals containing either low-fat (5% energy from fat) or high-fat (45% energy from fat) foods (Low-Fat and High-Fat groups, respectively). Each diet contained the same amount of carbohydrate and protein. An oral glucose tolerance test was performed the next morning. Muscle glycogen and intramuscular triglyceride (IMTG) concentrations were measured in muscle biopsy samples obtained immediately before exercise and the next morning. The day after exercise, muscle glycogen concentration was identical in High-Fat and Low-Fat (393 ± 70 and 379 ± 38 mmol/kg dry wt). At the same time, IMTG concentration was ∼20% greater during High-Fat compared with Low-Fat (42.5 ± 3.4 and 36.3 ± 3.3 mmol/kg dry wt; P < 0.05). Despite the addition of ∼165 g of fat to meals after exercise (∼1,500 kcal) and a resultant elevation in IMTG concentration, glucose tolerance was identical in High-Fat and Low-Fat (composite index: 8.7 ± 1.0 and 8.4 ± 1.0). In summary, as long as meals ingested in the hours after exercise contain the same carbohydrate content, the addition of ∼1,500 kcal from fat to these meals did not alter muscle glycogen resynthesis or glucose tolerance the next day.

Effects of elevated and exercise-reduced muscle glycogen levels on insulin sensitivity

1985 ◽  
Vol 59 (1) ◽  
pp. 154-159 ◽  
Author(s):  
J. L. Ivy ◽  
B. A. Frishberg ◽  
S. W. Farrell ◽  
W. J. Miller ◽  
W. M. Sherman
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Muscle Glycogen ◽  
Insulin Response ◽  
Tolerance Test ◽  
Exhaustive Exercise ◽  
Oral Glucose ◽  
Mixed Diet ◽  
Exercise Induced

The effects of an exercise-induced muscle glycogen reduction and an elevated muscle glycogen concentration on glucose tolerance and the insulin response to an oral glucose tolerance test (GTT) were examined. GTTs were administered to seven male subjects after 3 days on a mixed diet (C), after exhaustive exercise and 1 day on a high-fat protein diet (L-FP), after exhaustive exercise and 1 day on a mixed diet (L-M), and after exhaustive exercise and 3 days on a high-carbohydrate diet (H-CHO). The L-M treatment resulted in a significant reduction in muscle glycogen (C, 79.6 +/- 4.2 mmol/kg wet wt vs. L-M, 53.9 +/- 1.2 mmol/kg wet wt) and a 31.7% reduction in the insulin-glucose (IG) index, a measure of insulin sensitivity in vivo. Muscle glycogen was also significantly reduced by the L-FP treatment (49.1 +/- 2.4 mmol/kg wet wt), but there was no change in the IG index. Preventing a decrease in the IG index during the L-FP treatment may have been a result of elevated free fatty acids (67%) and ketones (552%) prior to the GTT. Muscle glycogen was significantly increased by the H-CHO treatment (124.8 +/- 11.1 mmol/kg wet wt); however, the IG index was not different from that of the C treatment. The results suggest that an exercise-induced reduction in muscle glycogen can improve insulin sensitivity in vivo but that this effect is diet dependent.

scholarly journals Insulin sensitivity obtained from the oral glucose tolerance test and its relationship with birthweight

2007 ◽  
Vol 27 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Yıldız Dallar ◽  
Dilek Dilli ◽  
Ilknur Bostancı ◽  
Elmas Öğüş ◽  
Şeyda Doğankoç ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance

scholarly journals Hypoglycemic effects and mechanisms of electroacupuncture on insulin resistance

2014 ◽  
Vol 307 (3) ◽  
pp. R332-R339 ◽  
Author(s):  
Jieyun Yin ◽  
Jian Kuang ◽  
Manisha Chandalia ◽  
Demidmaa Tuvdendorj ◽  
Batbayar Tumurbaatar ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Blood Glucose ◽  
Insulin Sensitivity ◽  
Free Fatty Acid ◽  
Glucose Tolerance ◽  
High Fat Diet ◽  
Postprandial Glucose ◽  
Tolerance Test ◽  
High Fat

The aim of this study was to investigate effects and mechanisms of electroacupuncture (EA) on blood glucose and insulin sensitivity in mice fed a high-fat diet. Both wild-type (WT) and adipose ectonucleotide pyrophosphate phosphodiesterase (ENPP1) transgenic (TG) mice were fed a high-fat diet for 12 wk; for each mouse, an intraperitoneal glucose tolerance test (IPGTT) and insulin tolerance test (ITT) were performed with or without EA at abdomen or auricular areas. A high-fat diet-induced insulin resistance in both WT and TG mice. In the WT mice, EA at 3 Hz and 15 Hz, but not at 1 Hz or 100 Hz, via CV4+CV12 significantly reduced postprandial glucose levels; EA at 3 Hz was most potent. The glucose level was reduced by 61.7% at 60 min and 74.5% at 120 min with EA at 3 Hz (all P < 0.001 vs. control). Similar hypoglycemic effect was noted in the TG mice. On the contrary, EA at auricular points increased postprandial glucose level ( P < 0.03). 4). EA at 3 Hz via CV4+CV12 significantly enhanced the decrease of blood glucose after insulin injection, suggesting improvement of insulin sensitivity. Plasma free fatty acid was significantly suppressed by 42.5% at 15 min and 50.8% at 30 min with EA ( P < 0.01) in both WT and TG mice. EA improves glucose tolerance in both WT and TG mice fed a high-fat diet, and the effect is associated with stimulation parameters and acupoints and is probably attributed to the reduction of free fatty acid.

scholarly journals Validation of Insulin Sensitivity Indices from Oral Glucose Tolerance Test Parameters in Obese Children and Adolescents

2004 ◽  
Vol 89 (3) ◽  
pp. 1096-1101 ◽  
Author(s):  
Catherine W. Yeckel ◽  
Ram Weiss ◽  
James Dziura ◽  
Sara E. Taksali ◽  
Sylvie Dufour ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Sensitivity Index ◽  
Intramyocellular Lipid ◽  
Insulin Sensitivity Index ◽  
Obese Youth ◽  
Intramyocellular Lipid Content

Abstract Given the extreme increase in prediabetes, type 2 diabetes, and the potential for metabolic syndrome in obese youth, identifying simplified indexes for assessing stimulated insulin sensitivity is critical. The purpose of this study was validation of two surrogate indexes of insulin sensitivity determined from the oral glucose tolerance test (OGTT): the composite whole body insulin sensitivity index (WBISI) and the insulin sensitivity index (ISI). An obese population (aged 8–18 yr) of normal and impaired glucose tolerance individuals was studied. One group (n = 38) performed both the euglycemic-hyperinsulinemic clamp and OGTT for comparison of insulin sensitivity measurements as well as 1H-magnetic resonance spectroscopy estimates of intramyocellular lipid content. Another larger (n = 368) cohort participated only in an OGTT. Both the WBISI and ISI represented good estimates (r = 0.78 and 0.74; P &lt; 0.0005) for clamp-derived insulin sensitivity (glucose disposed, M-value), respectively. In the large cohort, the surrogate indexes demonstrated the shift toward poorer function and increased risk profile as a function of insulin resistance. Additionally, the WBISI and ISI correlated with intramyocellular lipid content (r = −0.74 and −0.71; P &lt; 0.0001), a tissue marker for insulin resistance. Insulin sensitivity can be estimated using plasma glucose and insulin responses derived from the OGTT in obese youth with normal and impaired glucose tolerance.

Estimation of β-cell function from the data of the oral glucose tolerance test

2007 ◽  
Vol 292 (6) ◽  
pp. E1575-E1580 ◽  
Author(s):  
Shinji Sakaue ◽  
Shinji Ishimaru ◽  
Daisuke Ikeda ◽  
Yoshinori Ohtsuka ◽  
Toshiro Honda ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Tolerance ◽  
Glucose Tolerance Test ◽  
Cell Function ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Sensitivity Index ◽  
Β Cell ◽  
Β Cell Function ◽  
The Relationship

Although a hyperbolic relationship between insulin secretion and insulin sensitivity has been shown, the relationship has been often questioned. We examined the relationship using oral glucose tolerance test (OGTT)-derived indexes. A total of 374 Japanese subjects who had never been given a diagnosis of diabetes underwent a 75-g OGTT. In subjects with normal glucose tolerance (NGT), the ln [insulinogenic index (IGI)] was described by a linear function of ln ( x) ( x, insulin sensitivity index) in regression analysis when the reciprocal of the insulin resistance index in homeostasis model assessment, Matsuda's index, and oral glucose insulin sensitivity index were used as x. Because the 95% confidence interval of the slope of the regression line did not necessarily include −1, the relationships between IGI and x were not always hyperbolic, but power functions IGI × xα = a constant. We thought that IGI × xα was an appropriate β-cell function estimate adjusted by insulin sensitivity and referred to it as β-cell function index (BI). When Matsuda's index was employed as x, the BI values were decreased in subjects without NGT. Log BI had a better correlation with fasting plasma glucose (PG; FPG) and 2-h PG in non-NGT subjects than in NGT subjects. In subjects with any glucose tolerance, log BI was linearly correlated with 1-h PG and glucose spike (the difference between maximum PG and FPG). In conclusion, the relationship between insulin secretion and insulin sensitivity was not always hyperbolic. The BI is a useful tool in the estimation of β-cell function with a mathematical basis.

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