Effect of exercise training on insulin sensitivity and glucose metabolism in lean, obese, and diabetic men

1991 ◽  
Vol 71 (6) ◽  
pp. 2402-2411 ◽  
Author(s):  
K. R. Segal ◽  
A. Edano ◽  
A. Abalos ◽  
J. Albu ◽  
L. Blando ◽  
...  
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Exercise Training ◽  
Cardiorespiratory Fitness ◽  
Insulin Action ◽  
Training Session ◽  
Hepatic Glucose ◽  
Glucose Output

To clarify the impact of vigorous physical training on in vivo insulin action and glucose metabolism independent of the intervening effects of concomitant changes in body weight and composition and residual effects of an acute exercise session, 10 lean, 10 obese, and 6 diet-controlled type II diabetic men trained for 12 wk on a cycle ergometer 4 h/wk at approximately 70% of maximal O2 uptake (VO2max) while body composition and weight were maintained by refeeding the energy expended in each training session. Before and 4–5 days after the last training session, euglycemic hyperinsulinemic (40 mU.m2.min-1) clamps were performed at a plasma glucose of 90 mg/dl, combined with indirect calorimetry. Total insulin-stimulated glucose disposal (M) was corrected for residual hepatic glucose output. Body weight, fat, and fat-free mass (FFM) did not change with training, but cardiorespiratory fitness increased by 27% in all groups. Before and after training, M was lower for the obese (5.33 +/- 0.39 mg.kg FFM-1.min-1 pretraining; 5.33 +/- 0.46 posttraining) than for the lean men (9.07 +/- 0.49 and 8.91 +/- 0.60 mg.kg FFM-1.min-1 for pretraining and posttraining, respectively) and lower for the diabetic (3.86 +/- 0.44 and 3.49 +/- 0.21) than for the obese men (P less than 0.001). Insulin sensitivity was not significantly altered by training in any group, but basal hepatic glucose production was reduced by 22% in the diabetic men. Thus, when intervening effects of the last exercise bout or body composition changes were controlled, exercise training per se leading to increased cardiorespiratory fitness had no independent impact on insulin action and did not improve the insulin resistance in obese or diabetic men.

Preserved direct hepatic insulin action in rats with diet-induced hepatic steatosis

2004 ◽  
Vol 286 (5) ◽  
pp. E828-E833 ◽  
Author(s):  
Roland Buettner ◽  
Iris Ottinger ◽  
Jürgen Schölmerich ◽  
L. Cornelius Bollheimer
Keyword(s):  
Insulin Sensitivity ◽  
Hepatic Steatosis ◽  
Insulin Action ◽  
Glycogen Synthase ◽  
Hepatic Glucose Output ◽  
Hepatic Insulin Sensitivity ◽  
Significant Difference ◽  
Hepatic Glucose ◽  
Glucose Output

Recent in vivo studies have demonstrated a strong negative correlation between liver triglyceride content and hepatic insulin sensitivity, but a causal relationship remains to be established. We therefore have examined parameters of direct hepatic insulin action on isolated steatotic livers from high-fat (HF)-fed rats compared with standard chow (SC)-fed controls. Direct hepatic action of insulin was assayed in Wistar rats after 6 wk of HF diet by measuring the insulin-induced suppression of epinephrine-induced hepatic glucose output in an isolated liver perfusion system. Insulin-induced activation of glycogen synthase was measured by quantifying the incorporation of radioactive UDP-glucose into glycogen in HF and SC liver lysates. HF diet induced visceral obesity, mild insulin resistance, and hepatic steatosis. Both suppression of epinephrine-induced glycogenolysis and activation of glycogen synthase by insulin were sustained in HF rats; no significant difference from SC controls could be detected. In conclusion , in our model, triglyceride accumulation into the liver was not sufficient to impair direct hepatic insulin action. The data argue for an important role of systemic factors in the regulation of hepatic glucose output and hepatic insulin sensitivity in vivo.

scholarly journals Contribution of Gestational Weight Gain on Maternal Glucose Metabolism in Women with GDM and Normal Glucose Tolerance

2020 ◽  
Author(s):  
Fernanda L Alvarado ◽  
Perrie O’Tierney-Ginn ◽  
Patrick Catalano
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Weight Gain ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Normal Glucose Tolerance ◽  
Gestational Weight ◽  
Normal Glucose ◽  
The Relationship

Abstract Context Efforts to decrease the risk of developing metabolic complications of pregnancy such as gestational diabetes (GDM) through lifestyle intervention (decreasing excessive gestational weight gain (GWG)) during pregnancy have met with limited success. Objective The purpose of this study was to determine the relationship between the longitudinal changes in weight/body composition and insulin sensitivity and response in women with normal glucose tolerance (NGT) and those who developed GDM. Design We conducted a secondary analysis of a prospective cohort developed before conception and again at 34-36 weeks gestation. Twenty-nine NGT and seventeen GDM women were evaluated for longitudinal changes in insulin sensitivity/response using the hyperinsulinemic-euglycemic clamp and an IV-glucose tolerance test. Body composition was estimated using hydrodensitometry. Both absolute (Δ) and relative change (%Δ) between these two time points were calculated. We performed simple and multiple linear regression analysis to assess the relationship between GWG and measures of glucose metabolism, i.e. insulin sensitivity and response. Results Based on the primary study design there was no significant difference in clinical characteristics between women with NGT and those developing GDM. Prior to pregnancy, women who developed GDM had lower insulin sensitivity levels (p=0.01) compared to NGT women. Absolute change and %Δ in insulin sensitivity/insulin response and body weight/body composition was not significantly different between NGT and GDM women. Changes in body weight contributed to only 9% of the Δ insulin sensitivity both in women developing GDM and NGT women. Conclusions These data suggest that other factors – such as maternal pre-pregnancy insulin sensitivity and placental derived factors affecting insulin sensitivity rather than maternal GWG account for the changes in glucose metabolism during human pregnancy.

Assessing the utility of cardiorespiratory fitness, visceral fat, and liver fat in predicting changes in insulin sensitivity beyond simple changes in body weight after exercise training in adolescents

2021 ◽  
Vol 46 (1) ◽  
pp. 55-62
Author(s):  
Jennifer L. Kuk ◽  
SoJung Lee
Keyword(s):  
Body Composition ◽  
Body Weight ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Glucose Tolerance ◽  
Weight Change ◽  
Visceral Fat ◽  
Liver Fat ◽  
Body Weight Change ◽  
Sensitivity Changes

To examine the utility of changes in cardiorespiratory fitness (CRF) and body composition in response to exercise training in adolescents with obesity beyond simple measures of body weight change. This is a secondary analysis of our previously published randomized trials of aerobic, resistance, and combined training. We included 104 adolescents (body mass index (BMI) ≥85th percentile) who had complete baseline and post-intervention data for CRF, regional body fat, insulin sensitivity, and oral glucose tolerance. Associations between changes in body composition and CRF with cardiometabolic variables were examined adjusted for age, sex, Tanner stage, race, exercise group, and weight loss. At baseline, CRF, visceral fat and liver fat were correlated with insulin sensitivity with and without adjustment for BMI percentile. Training-associated changes in CRF, visceral fat, and liver fat were also correlated with insulin sensitivity changes, but not independent of body weight change. After accounting for body weight change, none of the body composition or CRF were associated with changes in insulin sensitivity, glucose tolerance, systolic blood pressure, or high-density lipoprotein cholesterol. Although CRF and body composition were strong independent correlates of insulin sensitivity at baseline, changes in CRF and visceral fat were not associated with changes in insulin sensitivity after accounting for body weight change. Clinicaltrials.gov registration nos.: NCT00739180, NCT01323088, NCT01938950. Novelty With exercise training, changes in body weight, CRF, visceral fat, and liver fat were correlated with changes in insulin sensitivity. Changes in body composition or CRF generally did not remain significant correlates of changes in insulin sensitivity after adjusting for body weight changes.

scholarly journals Effects of 7 days of exercise training on insulin sensitivity and responsiveness in type 2 diabetes mellitus

2009 ◽  
Vol 297 (1) ◽  
pp. E151-E156 ◽  
Author(s):  
John P. Kirwan ◽  
Thomas P. J. Solomon ◽  
Daniel M. Wojta ◽  
Myrlene A. Staten ◽  
John O. Holloszy
Keyword(s):  
Type 2 Diabetes ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Insulin Action ◽  
Insulin Infusion ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Short Term ◽  
Hepatic Glucose

The objectives of this study were to determine whether 1) the improvement in insulin action induced by short-term exercise training in patients with type 2 diabetes is due to an improvement in insulin sensitivity, an improvement in insulin responsiveness, or a combination of improved insulin sensitivity and responsiveness and 2) short-term exercise training results in improved suppression of hepatic glucose production by insulin. Fourteen obese patients with type 2 diabetes, age 64 ± 2 yr, underwent a two-stage hyperinsulinemic euglycemic clamp procedure, first stage 40 mU·m−2·min−1 insulin infusion, second stage 1,000 mU·m−2·min−1 insulin infusion, together with a [3-3H]glucose infusion, before and after 7 days of exercise. The training consisted of 30 min of cycling and 30 min of treadmill walking at ∼70% of maximal aerobic capacity daily for 7 days. The exercise program resulted in improvements in insulin action in the absence of weight loss. Glucose disposal rates during the euglycemic clamp were significantly increased at both hyperinsulinemic stages after training (40 mU: 1.84 ± 0.32 to 2.67 ± 0.37 mg·kg−1·min−1, P < 0.0001; 1,000 mU: 7.57 ± 0.61 to 8.84 ± 0.56 mg·kg−1·min−1, P = 0.008). Hepatic glucose production, both in the basal state (3.17 ± 0.43 vs. 2.54 ± 0.26 mg·kg−1·min−1, P = 0.05) and during the 40-mU clamp stage (1.15 ± 0.41 vs. 0.46 ± 0.20 mg·kg−1·min−1, P = 0.03), was significantly reduced after training. One week of vigorous exercise training can induce significant improvements in insulin action in type 2 diabetes. These improvements include increased peripheral insulin sensitivity and responsiveness as well as enhanced suppression of hepatic glucose production.

scholarly journals Cardiorespiratory Fitness and Diet Quality Profile of the Lithuanian Team of Deaf Women’s Basketball Players

2020 ◽  
Vol 17 (18) ◽  
pp. 6749
Author(s):  
Marius Baranauskas ◽  
Valerija Jablonskienė ◽  
Jonas Algis Abaravičius ◽  
Rimantas Stukas
Keyword(s):  
Vitamin D ◽  
Body Composition ◽  
Body Weight ◽  
Cardiorespiratory Fitness ◽  
Female Athletes ◽  
The Body ◽  
Physical Working Capacity ◽  
Working Capacity ◽  
Women's Basketball ◽  
Basketball Team

There are about 466 million people with hearing impairments in the world. The scientific literature does not provide sufficient data on the actual nutrition and other variables of professional deaf athletes. The objectives of this study were to investigate and evaluate the body composition, the physical working capacity, the nutrition intake, and the blood parameters of iron and vitamin D in the Lithuanian high-performance deaf women’s basketball team players. The female athletes (n = 14) of the Lithuanian deaf basketball team aged 26.4 ± 4.5 years were recruited for an observational cross-sectional study. A 7-day food recall survey method was used to investigate their actual diet. The measurements of the body composition were performed using the BIA (bioelectrical impedance analysis) tetra-polar electrodes. In order to assess the cardiorespiratory and aerobic fitness levels of athletes, ergo-spirometry (on a cycle ergometer) was used to measure the peak oxygen uptake (VO2peak) and the physical working capacity at a heart rate of 170 beats per minute (PWC170). The athletes’ blood tests were taken to investigate the red blood cells, hemoglobin, 25-hydroxyvitamin D, ferritin, transferrin, iron concentrations, and total iron-binding capacity (TIBC). The consideration of the VO2peak (55.9 ± 6.1 mL/min/kg of body weight, 95% CI: 51.8, 58.9) and the low VO2peak (56–60 mL/min/kg of body weight) (p = 0.966) in the deaf women’s basketball team players revealed no differences. For the deaf female athletes, the PWC170 was equal to 20.3 ± 2.0 kgm/min/kg of body weight and represented only the average aerobic fitness level. The carbohydrate and protein intakes (5.0 ± 1.3 and 1.3 ± 0.3 g/kg of body weight, respectively) met only the minimum levels recommended for athletes. The fat content of the diet (38.1 ± 4.1% of energy intake) exceeded the maximum recommended content (35% of energy intake) (p = 0.012). The mean blood serum concentrations of 25(OH)D and ferritin (24.1 ± 6.6 nmol/L and 11.0 ± 4.1 µg/L, respectively) predicted vitamin D and iron deficits in athletes. Female athletes had an increased risk of vitamin D and iron deficiencies. Regardless of iron deficiency in the body, the better cardiorespiratory fitness of the deaf female athletes was essentially correlated with the higher skeletal muscle mass (in terms of size) (r = 0.61, p = 0.023), the lower percentage of body fat mass (r = −0.53, p = 0.049), and the reduced intake of fat (r = −0.57, p = 0.040).

scholarly journals Exercise training reduces fatty acid availability and improves the insulin sensitivity of glucose metabolism

Diabetologia ◽  
2006 ◽  
Vol 50 (2) ◽  
pp. 404-413 ◽  
Author(s):  
F. Shojaee-Moradie ◽  
K. C. R. Baynes ◽  
C. Pentecost ◽  
J. D. Bell ◽  
E. L. Thomas ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Exercise Training

Effects of obesity and ovarian steroids on insulin secretion and removal in sheep

1989 ◽  
Vol 256 (1) ◽  
pp. E116-E128 ◽  
Author(s):  
J. P. McCann ◽  
E. N. Bergman ◽  
T. J. Reimers
Keyword(s):  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Plasma Concentrations ◽  
Tolerance Test ◽  
Intravenous Glucose Tolerance Test ◽  
Interactive Effects ◽  
Intravenous Glucose ◽  
Hepatic Glucose ◽  
Organ Removal ◽  
Glucose Output

The interactive effects of sex steroids and obesity on glucose metabolism and pancreatic secretion and organ removal of insulin were determined in multicatheterized lean and obese sheep by multiplying venoarterial concentration differences by plasma flows. Ovariectomized lean and dietary obese ewes received implants of progesterone and estradiol-17 beta that produced plasma concentrations of each equivalent to those during either anestrus (low progesterone), diestrus or pregnancy (high progesterone), or estrus (high estradiol). Sheep were exposed to each of the three steroid treatments for 2 days and fasted overnight before blood samples were collected for 5 h before (basal) and 90 min after injecting glucose (200 mg/kg) to simulate an intravenous glucose tolerance test (IVGTT). Regardless of steroid treatment, pancreatic secretory (18 vs. 5 mU/min) and hepatic (10 vs. 2 mU/min) and hindquarters (1.8 vs. 0.5 mU/min) removal rates of insulin in the basal state were greater (P less than 0.005) in obese than lean sheep. Obese sheep had greater (P less than 0.025) basal hepatic glucose output (66 vs. 47 mg/min) and similar hindquarters glucose removal (37 vs. 32 mg/min) as lean sheep even though arterial concentrations of insulin were fourfold higher (25 vs. 6 microU/ml; P less than 0.01) in the obese sheep. High progesterone increased (P less than 0.05) basal hepatic insulin removal in obese sheep. High progesterone and high estradiol increased insulin but decreased (P less than 0.05) glucose removal in hindquarters of obese sheep in the basal state. High progesterone potentiated significantly glucose-induced hyperinsulinemia in obese sheep, whereas high estradiol suppressed hepatic insulin removal but increased the removal of insulin by hindquarters during glucose stimulation in the obese sheep. We concluded that excessive insulin secretion, not decreased insulin removal, maintains the basal hyperinsulinemia in moderately obese sheep and that the progesterone-to-estradiol ratio has marked and divergent effects on insulin and glucose metabolism in individual tissues of sheep both in the basal state and during an IVGTT.

Effect of needle biopsy from the vastus lateralis muscle on insulin-stimulated glucose metabolism in humans

1994 ◽  
Vol 267 (4) ◽  
pp. E544-E548 ◽  
Author(s):  
P. Holck ◽  
N. Porksen ◽  
M. F. Nielsen ◽  
B. Nyholm ◽  
J. F. Bak ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Muscle Biopsy ◽  
Needle Biopsy ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Vastus Lateralis Muscle ◽  
Lateralis Muscle ◽  
Glucose Output

To examine the cellular mechanisms behind conditions characterized by insulin resistance, the clamp technique is often combined with muscle biopsies. To test whether the trauma of a needle biopsy from the vastus lateralis muscle per se may influence insulin-stimulated glucose uptake, eight healthy subjects underwent two randomly sequenced hyperinsulinemic (insulin infusion rate: 0.6 mU.kg-1.min-1 for 150 min) euglycemic clamps with an interval of 4-6 wk. In one study (study B) a muscle biopsy (approximately 250 mg, i.e., larger than normal standard) was taken in the basal state just before the clamp procedure, whereas the other was a control study (study C). Insulin-stimulated glucose uptake was significantly reduced in study B (5.36 +/- 0.96 mg.kg-1.min-1) compared with study C (6.06 +/- 0.68 mg.kg-1.min-1; P < 0.05). Nonoxidative glucose disposal (indirect calorimetry) was decreased (2.81 +/- 1.08 vs. 3.64 +/- 1.34 mg.kg-1.min-1; P < 0.05), whereas glucose oxidation was unaltered. Likewise, endogenous glucose output ([3-3H]glucose) was identically suppressed during hyperinsulinemia. Circulating levels of epinephrine, glucagon, and growth hormone did not differ significantly in studies B and C. In contrast, plasma norepinephrine, serum cortisol, and free fatty acid rose after biopsy (P < 0.05). In conclusion, performance of a muscle biopsy may diminish insulin sensitivity by affecting nonoxidative glucose metabolism. This should be considered when assessing whole body insulin sensitivity after a percutaneous needle muscle biopsy.

scholarly journals Arrestin domain-containing 3 (Arrdc3) modulates insulin action and glucose metabolism in liver

2020 ◽  
Vol 117 (12) ◽  
pp. 6733-6740 ◽  
Author(s):  
Thiago M. Batista ◽  
Sezin Dagdeviren ◽  
Shannon H. Carroll ◽  
Weikang Cai ◽  
Veronika Y. Melnik ◽  
...  
Keyword(s):  
Messenger Rna ◽  
Insulin Action ◽  
Hepatic Glucose Production ◽  
Glycogen Synthesis ◽  
Glucose Production ◽  
Hepatic Glycogen ◽  
Glycogen Accumulation ◽  
Hepatic Glucose ◽  
Glucose Output

Insulin action in the liver is critical for glucose homeostasis through regulation of glycogen synthesis and glucose output. Arrestin domain-containing 3 (Arrdc3) is a member of the α-arrestin family previously linked to human obesity. Here, we show thatArrdc3is differentially regulated by insulin in vivo in mice undergoing euglycemic-hyperinsulinemic clamps, being highly up-regulated in liver and down-regulated in muscle and fat. Mice with liver-specific knockout (KO) of the insulin receptor (IR) have a 50% reduction inArrdc3messenger RNA, while, conversely, mice with liver-specific KO ofArrdc3(L-Arrdc3KO) have increased IR protein in plasma membrane. This leads to increased hepatic insulin sensitivity with increased phosphorylation of FOXO1, reduced expression of PEPCK, and increased glucokinase expression resulting in reduced hepatic glucose production and increased hepatic glycogen accumulation. These effects are due to interaction of ARRDC3 with IR resulting in phosphorylation of ARRDC3 on a conserved tyrosine (Y382) in the carboxyl-terminal domain. Thus,Arrdc3is an insulin target gene, and ARRDC3 protein directly interacts with IR to serve as a feedback regulator of insulin action in control of liver metabolism.

Alterations in basal glucose metabolism during late pregnancy in the conscious dog

2000 ◽  
Vol 279 (5) ◽  
pp. E1166-E1177 ◽  
Author(s):  
Cynthia C. Connolly ◽  
Linda C. Holste ◽  
Lisa N. Aglione ◽  
Doss W. Neal ◽  
D. Brooks Lacy ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Hepatic Glucose Production ◽  
Late Pregnancy ◽  
Nonesterified Fatty Acid ◽  
Acid Uptake ◽  
Substrate Uptake ◽  
Hepatic Glucose Output ◽  
Hepatic Glucose ◽  
Glucose Output ◽  
In Pregnancy

We assessed basal glucose metabolism in 16 female nonpregnant (NP) and 16 late-pregnant (P) conscious, 18-h-fasted dogs that had catheters inserted into the hepatic and portal veins and femoral artery ∼17 days before the experiment. Pregnancy resulted in lower arterial plasma insulin (11 ± 1 and 4 ± 1 μU/ml in NP and P, respectively, P < 0.05), but plasma glucose (5.9 ± 0.1 and 5.6 ± 0.1 mg/dl in NP and P, respectively) and glucagon (39 ± 3 and 36 ± 2 pg/ml in NP and P, respectively) were not different. Net hepatic glucose output was greater in pregnancy (42.1 ± 3.1 and 56.7 ± 4.0 μmol · 100 g liver−1· min−1in NP and P, respectively, P < 0.05). Total net hepatic gluconeogenic substrate uptake (lactate, alanine, glycerol, and amino acids), a close estimate of the gluconeogenic rate, was not different between the groups (20.6 ± 2.8 and 21.2 ± 1.8 μmol · 100 g liver−1· min−1in NP and P, respectively), indicating that the increment in net hepatic glucose output resulted from an increase in the contribution of glycogenolytically derived glucose. However, total glycogenolysis was not altered in pregnancy. Ketogenesis was enhanced nearly threefold by pregnancy (6.9 ± 1.2 and 18.2 ± 3.4 μmol · 100 g liver−1· min−1in NP and P, respectively), despite equivalent net hepatic nonesterified fatty acid uptake. Thus late pregnancy in the dog is not accompanied by changes in the absolute rates of gluconeogenesis or glycogenolysis. Rather, repartitioning of the glucose released from glycogen is responsible for the increase in hepatic glucose production.

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