scholarly journals A Lowly Digestible-Starch Diet after Weaning Enhances Exogenous Glucose Oxidation Rate in Female, but Not in Male, Mice

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2242
Author(s):  
José M. S. Fernández-Calleja ◽  
Lianne M. S. Bouwman ◽  
Hans J. M. Swarts ◽  
Nils Billecke ◽  
Annemarie Oosting ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Hydrogen Production ◽  
Glucose Oxidation ◽  
Amylase Activity ◽  
Whole Body ◽  
Total Carbohydrate ◽  
Exogenous Glucose ◽  
13C Label ◽  
Body Energy ◽  
Starch Diet

Starches of low digestibility are associated with improved glucose metabolism. We hypothesise that a lowly digestible-starch diet (LDD) versus a highly digestible-starch diet (HDD) improves the capacity to oxidise starch, and that this is sex-dependent. Mice were fed a LDD or a HDD for 3 weeks directly after weaning. Body weight (BW), body composition (BC), and digestible energy intake (dEI) were determined weekly. At the end of the intervention period, whole-body energy expenditure (EE), respiratory exchange ratio (RER), hydrogen production, and the oxidation of an oral 13C-labelled starch bolus were measured by extended indirect calorimetry. Pancreatic amylase activity and total 13C hepatic enrichment were determined in females immediately before and 4 h after administration of the starch bolus. For both sexes, BW, BC, and basal EE and RER were not affected by the type of starch, but dEI and hydrogen production were increased by the LDD. Only in females, total carbohydrate oxidation and starch-derived glucose oxidation in response to the starch bolus were higher in LDD versus HDD mice; this was not accompanied by differences in amylase activity or hepatic partitioning of the 13C label. These results show that starch digestibility impacts glucose metabolism differently in females versus males.

High Pancreatic Amylase Expression Promotes Adiposity in Obesity-Prone Carbohydrate-Sensitive Rats

2019 ◽  
Vol 149 (2) ◽  
pp. 270-279 ◽  
Author(s):  
Dalila Azzout-Marniche ◽  
Catherine Chaumontet ◽  
Julien Piedcoq ◽  
Nadezda Khodorova ◽  
Gilles Fromentin ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Glucose Oxidation ◽  
Amylase Activity ◽  
Whole Body ◽  
Amylase Secretion ◽  
Low Fat ◽  
Adipose Tissues ◽  
High Starch ◽  
Dietary Starch ◽  
Starch Diet

ABSTRACT Background We have reported large differences in adiposity (fat mass/body weight) gain between rats fed a low-fat, high-starch diet, leading to their classification into carbohydrate “sensitive” and “resistant” rats. In sensitive animals, fat accumulates in visceral adipose tissues, leading to the suggestion that this form of obesity could be responsible for rapid development of metabolic syndrome. Objective We investigated whether increased amylase secretion by the pancreas and accelerated starch degradation in the intestine could be responsible for this phenotype. Method Thirty-two male Wistar rats (7-wk-old) were fed a purified low-fat (10%), high-carbohydrate diet for 6 wk, in which most of the carbohydrate (64% by energy) was provided as corn starch. Meal tolerance tests of the Starch diet were performed to measure glucose and insulin responses to meal ingestion. Indirect calorimetry combined with use of 13C-labelled dietary starch was used to assess meal-induced changes in whole body and starch-derived glucose oxidation. Real-time polymerase chain reaction was used to assess mRNA expression in pancreas, liver, white and brown adipose tissues, and intestine. Amylase activity was measured in the duodenum, jejunum, and ileum contents. ANOVA and regression analyses were used for statistical comparisons. Results “Resistant” and “sensitive” rats were separated according to adiposity gain during the study (1.73% ± 0.20% compared with 4.35% ± 0.36%). Breath recovery of 13CO2 from 13C-labelled dietary starch was higher in “sensitive” rats, indicating a larger increase in whole body glucose oxidation and, conversely, a larger decrease in lipid oxidation. Amylase mRNA expression in pancreas, and amylase activity in jejunum, were also higher in sensitive rats. Conclusion Differences in digestion of starch can promote visceral fat accumulation in rats when fed a low-fat, high-starch diet. This mechanism may have important implications in human obesity.

scholarly journals Acute Hypoxia Suppresses Exogenous Glucose Oxidation, Lowers Fat Oxidation, and Increases Muscle Glycogenolysis During Steady-state Aerobic Exercise (P08-084-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Lee Margolis ◽  
Marques Wilson ◽  
Claire Whitney ◽  
Christopher Carrigan ◽  
Nancy Murphy ◽  
...  
Keyword(s):  
Steady State ◽  
Aerobic Exercise ◽  
Glucose Oxidation ◽  
Acute Hypoxia ◽  
Fat Oxidation ◽  
Carbohydrate Oxidation ◽  
Hepatic Glycogen ◽  
Total Carbohydrate ◽  
Carbohydrate Ingestion ◽  
Exogenous Glucose

Abstract Objectives Lowlanders performing steady-state aerobic exercise during high-altitude (HA) sojourns, hypoxia mediates increased endogenous carbohydrate oxidation compared to sea level (SL). At SL, ingesting carbohydrate during exercise spares endogenous carbohydrate stores and improves endurance. However, it is unclear whether that strategy is effective at HA, as data from a recent study suggests exogenous glucose oxidation is suppressed during aerobic exercise performed 5 hr after arriving at HA. This observation has not been replicated. The objective of this study was to determine substrate oxidative responses to exogenous carbohydrate ingestion during steady-state aerobic exercise at SL and HA. Methods Using a randomized, crossover design, native lowlanders (n = 8 males, mean ± SD, age: 23 ± 2 yr, body mass: 87 ± 10 kg, and VO2peak: SL 4.3 ± 0.2 L/min and HA 2.9 ± 0.2 L/min) consumed 145 g (1.8 g/min) of glucose while performing 80 min of metabolically-matched (SL: 1.66 ± 0.14 L/min 347 ± 29 kcal, HA: 1.59 ± 0.10 L/min, 369 ± 39 kcal) treadmill exercise at SL (757 mmHg) and HA (460 mmHg) conditions after a 5 hr exposure. Total carbohydrate and fat oxidation rates (g/min) during exercise were determined by indirect calorimetry, and exogenous, muscle- and hepatic-derived glucose oxidation by tracer technique using breath and blood measurements of 13C-glucose. Results Total carbohydrate oxidation was higher (P < 0.05) at HA (2.15 ± 0.32) compared to SL (1.39 ± 0.14). Exogenous glucose oxidation was lower (P < 0.05) at HA (0.35 ± 0.07) than SL (0.44 ± 0.05). Muscle glycogen oxidation was higher at HA (1.67 ± 0.26) compared to SL (0.83 ± 0.13). There was no difference in hepatic glycogen oxidation between SL (0.13 ± 0.03) and HA (0.13 ± 0.04). Fat oxidation was lower at HA (0.05 ± 0.07) than SL (0.31 ± 0.08). Conclusions These data confirm that acute hypoxic exposure suppresses exogenous carbohydrate oxidation during steady-state exercise. Coupled with observations that fat oxidation was reduced and muscle glycogenolysis accelerated in hypoxia, these findings suggest that ingesting carbohydrate during exercise upon acute hypoxia exposure is not an effective strategy for attenuating oxidation of endogenous carbohydrate stores. Funding Sources Views expressed are the authors and do not reflect the official policy of the Army, DoD, or the U.S. Government. Supported by USAMRMC.

Effect of IL-6 on the insulin sensitivity in patients with type 2 diabetes

2014 ◽  
Vol 306 (7) ◽  
pp. E769-E778 ◽  
Author(s):  
N. M. Harder-Lauridsen ◽  
R. Krogh-Madsen ◽  
J. J. Holst ◽  
P. Plomgaard ◽  
L. Leick ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Whole Body ◽  
Cytokine Signaling ◽  
Contributing Factors ◽  
Stat3 Phosphorylation ◽  
Socs3 Expression ◽  
Body Energy

Elevated interleukin-6 (IL-6) levels are associated with type 2 diabetes, but its role in glucose metabolism is controversial. We investigated the effect of IL-6 on insulin-stimulated glucose metabolism in type 2 diabetes patients and hypothesized that an acute, moderate IL-6 elevation would increase the insulin-mediated glucose uptake. Men with type 2 diabetes not treated with insulin [ n = 9, age 54.9 ± 9.7 (mean ± SD) yr, body mass index 34.8 ± 6.1 kg/m2, HbA1c7.0 ± 1.0%] received continuous intravenous infusion with either recombinant human IL-6 (rhIL-6) or placebo. After 1 h with placebo or rhIL-6, a 3-h hyperinsulinemic-isoglycemic clamp was initiated. Whole body glucose metabolism was measured using stable isotope-labeled tracers. Signal transducer and activator of transcription 3 (STAT3) phosphorylation and suppressor of cytokine signaling 3 (SOCS3) expression were measured in muscle biopsies. Whole body energy expenditure was measured using indirect calorimetry. In response to the infusion of rhIL-6, circulating levels of IL-6 ( P < 0.001), neutrophils ( P < 0.001), and cortisol ( P < 0.001) increased while lymphocytes decreased ( P < 0.01). However, IL-6 infusion did not change glucose infusion rate, rate of appearance, or rate of disappearance during the clamp. While IL-6 enhanced phosphorylation of STAT3 in skeletal muscle ( P = 0.041), the expression of SOCS3 remained unchanged. Whole body oxygen uptake ( P < 0.01) and expired carbon dioxide ( P < 0.01) increased during rhIL-6 infusion. In summary, although IL-6 induced local and systemic responses, the insulin-stimulated glucose uptake was not affected. While different contributing factors may be involved, our results are in contrast to our hypothesis and previous findings in young, healthy men.

Remarkable metabolic availability of oral glucose during long-duration exercise in humans

1986 ◽  
Vol 60 (3) ◽  
pp. 1035-1042 ◽  
Author(s):  
N. Pallikarakis ◽  
B. Jandrain ◽  
F. Pirnay ◽  
F. Mosora ◽  
M. Lacroix ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Glucose Oxidation ◽  
Carbohydrate Oxidation ◽  
Oral Glucose ◽  
Total Carbohydrate ◽  
Carbohydrate Utilization ◽  
Exogenous Glucose ◽  
Long Duration ◽  
Glucose Ingestion ◽  
Exercise In Humans

It was reported previously that glucose ingestion prior to or at the beginning of muscular exercise was a readily available metabolic substrate. The aim of this study was to see what percentage of carbohydrate utilization can be covered by glucose ingested regularly during exercise. Male healthy volunteers exercised for 285 min at approximately 45% of their individual maximal O2 uptake on a 10% uphill treadmill. After 15 min adaptation to exercise they received either 200 g (group G 200) or 400 g (group G 400) glucose (0.25 g X ml H2O-1) orally in eight equal doses repeated every 30 min (G 200 = 8 X 25 g, n = 4; G 400 = 8 X 50 g, n = 4). Indirect calorimetry was used to evaluate carbohydrate and lipid oxidation. Naturally labeled [13C]glucose was used to follow the oxidation of the exogenous glucose. Total carbohydrate oxidation was 341 +/- 22 and 332 +/- 32 g, lipid oxidation was 119 +/- 8 and 105 +/- 5 g, and exogenous glucose oxidation was 137 +/- 4 and 227 +/- 13 g (P less than 0.005) in groups G 200 and G 400, respectively. Endogenous glucose oxidation was about half in G 400 of what it was in G 200: 106 +/- 27 vs. 204 +/- 24 g (P less than 0.02). During the last hour of exercise, exogenous oxidation represented 55.3 and 87.5% of total carbohydrate oxidation for groups G 200 and G 400, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic availability of glucose ingested 3 h before prolonged exercise in humans

1984 ◽  
Vol 56 (5) ◽  
pp. 1314-1319 ◽  
Author(s):  
B. Jandrain ◽  
G. Krzentowski ◽  
F. Pirnay ◽  
F. Mosora ◽  
M. Lacroix ◽  
...  
Keyword(s):  
Glucose Oxidation ◽  
Exercise Bout ◽  
Moderate Intensity ◽  
Total Carbohydrate ◽  
Exogenous Glucose ◽  
Plasma Insulin Levels ◽  
Exercise Induced ◽  
Total Glucose ◽  
Blood Glucose Concentrations ◽  
Exercise In Humans

The aim of the present study was to investigate the extent to which an oral load of glucose ingested 3 h before a 4-h exercise bout of moderate intensity represents an energy source readily available during that exercise. Therefore, five healthy male volunteers drank 100 g of naturally labeled [13C]glucose dissolved in 400 ml of water, rested for 3 h, and then exercised on a treadmill for the next 4 h at about 45% of their individual maximum O2 consumption. Total glucose oxidation was derived from nonprotein respiratory quotient and exogenous glucose oxidation evaluated by the 13C methodology as previously described. Total carbohydrate oxidation averaged 285 +/- 17 g during the 7 h of the test, the global amount of carbohydrate oxidized during the exercising period was 253.1 +/- 16.9 g/4 h. Exogenous glucose oxidation averaged 11.3 +/- 0.7 g during the 3-h period of rest and increased markedly after the beginning of exercise, reaching 18.9 +/- 2.2 g/30 min during the first 30 min of exercise; the total amount of exogenous glucose oxidized during the 4 h of exercise was 67.5 +/- 9.4 g. Throughout the whole period of exercise, blood glucose concentrations remained between 3.5 and 4.0 mmol/l. Exercise induced a major fall in plasma insulin levels that reached undetectable values after 3 and 4 h, whereas plasma glucagon levels tended to rise, but their level never significantly exceeded the basal values; plasma free fatty acids and glycerol increased markedly during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The mTORC1 complex in pre-osteoblasts regulates whole-body energy metabolism independently of osteocalcin

Bone Research ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Pawanrat Tangseefa ◽  
Sally K. Martin ◽  
Peck Yin Chin ◽  
James Breen ◽  
Chui Yan Mah ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Insulin Signaling ◽  
Skeletal Development ◽  
Critical Role ◽  
Lipid Absorption ◽  
Whole Body ◽  
Conditional Deletion ◽  
Insulin Dependent ◽  
Body Energy

AbstractOvernutrition causes hyperactivation of mTORC1-dependent negative feedback loops leading to the downregulation of insulin signaling and development of insulin resistance. In osteoblasts (OBs), insulin signaling plays a crucial role in the control of systemic glucose homeostasis. We utilized mice with conditional deletion of Rptor to investigate how the loss of mTORC1 function in OB affects glucose metabolism under normal and overnutrition dietary states. Compared to the controls, chow-fed Rptorob−/− mice had substantially less fat mass and exhibited adipocyte hyperplasia. Remarkably, upon feeding with high-fat diet, mice with pre- and post-natal deletion of Rptor in OBs were protected from diet-induced obesity and exhibited improved glucose metabolism with lower fasting glucose and insulin levels, increased glucose tolerance and insulin sensitivity. This leanness and resistance to weight gain was not attributable to changes in food intake, physical activity or lipid absorption but instead was due to increased energy expenditure and greater whole-body substrate flexibility. RNA-seq revealed an increase in glycolysis and skeletal insulin signaling pathways, which correlated with the potentiation of insulin signaling and increased insulin-dependent glucose uptake in Rptor-knockout osteoblasts. Collectively, these findings point to a critical role for the mTORC1 complex in the skeletal regulation of whole-body glucose metabolism and the skeletal development of insulin resistance.

scholarly journals Mechanisms of Whole-Body Glycogen Deposition after Oral Glucose in Normal Subjects. Influence of the Nutritional Status1

1998 ◽  
Vol 83 (8) ◽  
pp. 2810-2816
Author(s):  
F. Féry ◽  
L. Plat ◽  
E. O. Balasse
Keyword(s):  
Glucose Oxidation ◽  
Normal Subjects ◽  
Whole Body ◽  
Minor Role ◽  
Oral Glucose ◽  
Glycogen Depletion ◽  
Total Carbohydrate ◽  
Glucose Ingestion ◽  
Glycogen Deposition ◽  
A Minor

abstract It is known that prior fasting enhances whole-body glycogen retention after glucose ingestion. To identify the involved mechanisms, 33 normal volunteers underwent a total fast, varying between 14 h and 4 days, and ingested thereafter 75 g glucose labeled with[ 14C]-glucose. Measurements of oral glucose oxidation (expired 14CO2, corrected for incomplete recovery) and total carbohydrate (CHO) oxidation (indirect calorimetry) were performed over the following 5 h. These data allowed us to calculate oral glucose storage (uptake − oxidation), glycogen oxidation (CHO oxidation − oral glucose oxidation), and net CHO balance (oral glucose uptake − CHO oxidation). As compared with an overnight fast, prolonged fasting (4 days) inhibited the uptake (64.8 vs. 70.3 g/5 h; P &lt; 0.01) and the oxidation (10.9 vs. 20.0 g/5h; P&lt; 0.001) of oral glucose and stimulated slightly its conversion to glycogen (53.9 vs. 50.3 g/5 h; P &lt; 0.05). The latter effect played only a minor role in the marked increase in net CHO balance (52.3 vs. 25.2 g/5 h; P &lt; 0.001), which was almost entirely related to a decrease in glycogen oxidation (1.6 vs. 25.1 g/5 h; P &lt; 0.001). Considering the whole series of data, including intermediate durations of fast, it was observed that the modifications in postprandial CHO metabolism, induced by fasting, correlated strongly with basal CHO oxidation, suggesting that the degree of initial glycogen depletion is a major determinant of glycogen oxidation and net CHO storage. Thus, prior fasting stimulates postprandial glycogen retention, mainly through an inhibition of the glycogen turnover that exists in overnight-fasted subjects, during the absorptive period.

Effect of physical training on utilization of a glucose load given orally during exercise

1984 ◽  
Vol 246 (5) ◽  
pp. E412-E417 ◽  
Author(s):  
G. Krzentowski ◽  
F. Pirnay ◽  
A. S. Luyckx ◽  
M. Lacroix ◽  
F. Mosora ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Physical Training ◽  
Glucose Oxidation ◽  
Exercise Bout ◽  
Moderate Intensity ◽  
Glucose Load ◽  
Total Carbohydrate ◽  
Oxidation Rates ◽  
Exogenous Glucose ◽  
Glucose Ingestion

The effect of a 6-wk training period on the oxidation of a 100-g glucose load given orally during exercise was investigated in six healthy male volunteers. The subjects were submitted before and 24 h after the training program to a 105-min exercise bout (performed at about 40% of the pretraining VO2max) followed by a 90-min resting period. Naturally labeled [13C]glucose was given 15 min after the beginning of exercise. Exogenous glucose oxidation was derived from 13CO2 measurements in expired air, and total glucose and lipid oxidation were evaluated by indirect calorimetry. Training (60-min bicycling 5 days a week at 30-40% VO2max) resulted in a 29% increase in VO2max. During the 15 min of exercise that preceded glucose ingestion, the rate of total carbohydrate oxidation was slightly decreased after training, whereas the rate of lipid oxidation was slightly increased. Training did not affect the response of blood glucose, plasma insulin, or plasma free fatty acids to the glucose ingested during exercise; in contrast, the circulating levels of epinephrine, glycerol, and lactate were significantly reduced after training. Substrate utilization measurements revealed similar oxidation rates of carbohydrates (106.9 +/- 2.7 before vs. 100.2 +/- 4.7 g/3 h after training) and of lipids. However, detailed analysis revealed a significant 17% increase in exogenous glucose oxidation, thus indicating a significant sparing of endogenous carbohydrates. In conclusion, physical training induces a modest but significant increase in the oxidation of an oral load of glucose given during subsequent exercise of moderate intensity, a phenomenon reinforcing the sparing of endogenous carbohydrate stores.

Fate of exogenous glucose during exercise of different intensities in humans

1982 ◽  
Vol 53 (6) ◽  
pp. 1620-1624 ◽  
Author(s):  
F. Pirnay ◽  
J. M. Crielaard ◽  
N. Pallikarakis ◽  
M. Lacroix ◽  
F. Mosora ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Glucose Oxidation ◽  
Prolonged Exercise ◽  
Treadmill Exercise ◽  
Work Load ◽  
Intense Exercise ◽  
Vo2 Max ◽  
Total Carbohydrate ◽  
Exogenous Glucose ◽  
Adaptation To Exercise

The extent to which an oral load of glucose is absorbed from the gut and oxidized during prolonged exercise is a matter of controversy. Four healthy volunteers, 18–28 yr, were submitted on 4 different days to a 105-min treadmill exercise at 22, 39, 51, and 64% of their individual VO2max. After 15 min adaptation to exercise, they received orally 100 g naturally labeled [13C]glucose. Oxidation of the exogenous glucose was followed by 13CO2 measurements in the expired air; total carbohydrate and lipid oxidation were evaluated by indirect calorimetry. Between 22 and 51% VO2 max, total carbohydrate, lipid oxidation, and exogenous glucose oxidation were linearly correlated with the relative work load (r = 0.81; P less than 0.01). Between 51 and 64% VO2 max, exogenous glucose oxidation and lipid oxidation tended to level off, whereas endogenous carbohydrate oxidation was markedly enhanced. The lesser contribution of exogenous glucose during the most intense exercise might be due to a decrease in the oxidation in the muscles or to a lesser availability of this exogenous glucose.

Thermoneutral housing does not influence fat mass or glucose homeostasis in C57BL/6 mice

2018 ◽  
Vol 239 (3) ◽  
pp. 313-324 ◽  
Author(s):  
Lewin Small ◽  
Henry Gong ◽  
Christian Yassmin ◽  
Gregory J Cooney ◽  
Amanda E Brandon
Keyword(s):  
Glucose Metabolism ◽  
Ambient Temperature ◽  
Fat Mass ◽  
Glucose Homeostasis ◽  
Dietary Intervention ◽  
Whole Body ◽  
Housing Temperature ◽  
Brown Adipose ◽  
Normal Chow ◽  
Obesogenic Diet

One major factor affecting physiology often overlooked when comparing data from animal models and humans is the effect of ambient temperature. The majority of rodent housing is maintained at ~22°C, the thermoneutral temperature for lightly clothed humans. However, mice have a much higher thermoneutral temperature of ~30°C, consequently data collected at 22°C in mice could be influenced by animals being exposed to a chronic cold stress. The aim of this study was to investigate the effect of housing temperature on glucose homeostasis and energy metabolism of mice fed normal chow or a high-fat, obesogenic diet (HFD). Male C57BL/6J(Arc) mice were housed at standard temperature (22°C) or at thermoneutrality (29°C) and fed either chow or a 60% HFD for 13 weeks. The HFD increased fat mass and produced glucose intolerance as expected but this was not exacerbated in mice housed at thermoneutrality. Changing the ambient temperature, however, did alter energy expenditure, food intake, lipid content and glucose metabolism in skeletal muscle, liver and brown adipose tissue. Collectively, these findings demonstrate that mice regulate energy balance at different housing temperatures to maintain whole-body glucose tolerance and adiposity irrespective of the diet. Despite this, metabolic differences in individual tissues were apparent. In conclusion, dietary intervention in mice has a greater impact on adiposity and glucose metabolism than housing temperature although temperature is still a significant factor in regulating metabolic parameters in individual tissues.

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