Difference in leptin response to a high-fat meal between lean and obese men

2001 ◽  
Vol 101 (4) ◽  
pp. 359-365 ◽  
Author(s):  
P. IMBEAULT ◽  
E. DOUCET ◽  
P. MAURIÈGE ◽  
S. ST-PIERRE ◽  
C. COUILLARD ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Statistical Significance ◽  
Insulin Response ◽  
High Fat ◽  
Glucose Levels ◽  
Time Interaction ◽  
Fasting Plasma ◽  
Effect Of Food ◽  
Plasma Leptin ◽  
Fat Meal

The aim of this study was to compare the leptin responses to a high-fat meal in lean and obese men, and to investigate whether the net leptin response (area under the incremental curve) after the meal was related to the thermic effect of food (TEF). Blood samples were collected after an overnight fast and every 2h for 8h after a high-fat breakfast (60g of fat/m2 body surface area) in 12 lean and 12 obese men for determination of glucose, insulin and leptin. The TEF was calculated as postprandial energy expenditure minus fasting energy expenditure, as measured by indirect calorimetry. Fasting plasma glucose levels were similar in lean and obese men, and increased in the same way after the meal. Fasting and postprandial plasma insulin concentrations were significantly greater in obese than in lean men (P < 0.01 and P < 0.05 respectively). Accordingly, obese men showed a significantly higher net insulin response than lean subjects (P < 0.001). Fasting plasma leptin levels were greater in obese than in lean men (P < 0.001). After the meal, plasma leptin increased significantly in lean men, whereas it decreased in obese men (group by time interaction, P < 0.01). The net response of leptin was greater in lean than in obese men, but this did not reach statistical significance (P = 0.07). Moreover, the TEF was similar in the two groups. No significant relationship was observed between either the net insulin response or the net leptin response after the high-fat meal and the TEF of lean subjects (-0.05 < r < 0.31). In obese men, the net response of insulin was correlated significantly with TEF (r = 0.70, P < 0.05), whereas the net response of leptin was not (r = -0.40). These results suggest that obesity is related to an impaired regulation of leptin by insulin, since leptin levels increased in lean men but decreased in obese men following a high-fat meal. Moreover, the fact that the postprandial leptin responses of both lean and obese men were not significantly related to the TEF suggests that the ob gene product is probably not acutely involved in the control of this energy expenditure component in humans.

Effect of a high-fat diet on energy balance and thermic effect of food in hypothyroid rats

1997 ◽  
Vol 136 (3) ◽  
pp. 309-315 ◽  
Author(s):  
Susanna Iossa ◽  
Maria Pina Mollica ◽  
Lillà Lionetti ◽  
Antonio Barletta ◽  
Giovanna Liverini
Keyword(s):  
Energy Balance ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Thermic Effect Of Food ◽  
Effect Of Food ◽  
Thermic Effect ◽  
Fat Meal

Abstract We have carried out measurements of energy balance in hypothyroid rats fed a low-fat or a high-fat diet for eighteen days. We have also measured cephalic and processing thermic effect of food (TEF) after a low-fat or a high-fat meal. Body lipid gain, carcass lipid content and gross efficiency were significantly (P < 0·05) higher in hypothyroid rats fed a high-fat diet compared with hypothyroid rats fed a low-fat diet, while metabolizable energy intake and energy expenditure remained unchanged. Cephalic TEF after a low-fat meal was significantly (P < 005) lower in hypothyroid rats fed a high-fat diet compared with hypothyroid rats fed a low-fat diet, while it was significantly (P <0·05) higher after a high-fat meal than after a low-fat meal in hypothyroid rats fed a high-fat diet. No significant variation was found in processing TEF after a low-fat or a high-fat meal. Our results indicate that hypothyroid rats are unable to develop increased energy expenditure and increased TEF in response to a high-fat diet. European Journal of Endocrinology 136 309–315

The effect of acute fish-oil supplementation on endothelial function and arterial stiffness following a high-fat meal

2010 ◽  
Vol 35 (3) ◽  
pp. 294-302 ◽  
Author(s):  
Christopher A. Fahs ◽  
Huimin Yan ◽  
Sushant Ranadive ◽  
Lindy M. Rossow ◽  
Stamatis Agiovlasitis ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Endothelial Function ◽  
Fish Oil ◽  
Brachial Artery ◽  
Omega 3 ◽  
High Fat ◽  
Time Interaction ◽  
Artery Stiffness ◽  
Fish Oil Supplementation ◽  
Fat Meal

This study examined whether a commercially available fish-oil supplement offers protection from the acute effects of a high-fat meal (HFM) on endothelial function and arterial stiffness. An HFM causes acute impairments in endothelial function, whereas the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have a variety of cardioprotective effects. However, little is known about the efficacy of moderate fish-oil supplementation on the endothelial dysfunction induced by an HFM. Endothelial function (brachial artery flow-mediated dilation (FMD)), forearm blood flow (FBF), total hyperemia, central and peripheral blood pressure, and central artery stiffness were assessed in 20 healthy men (n = 10) and women (n = 10) at rest and 4 h after an HFM supplemented with either placebo or ∼1 g EPA and DHA. Brachial artery FMD normalized for shear rate was significantly impaired (p = 0.033) following the HFM with placebo but remained unchanged compared with baseline following the HFM with the fish-oil supplement (p = 0.039; condition × time interaction). Resting FBF (p = 0.020) and total hyperemia (p = 0.014) were elevated following the HFM. All other vascular and hemodynamic measurements were unchanged in both trials. Commercially available fish-oil supplements taken with an HFM appear to preserve endothelial function following an HFM.

Programmed metabolic syndrome: prenatal undernutrition and postweaning overnutrition

2007 ◽  
Vol 293 (6) ◽  
pp. R2306-R2314 ◽  
Author(s):  
Mina Desai ◽  
Jooby Babu ◽  
Michael G. Ross
Keyword(s):  
Metabolic Syndrome ◽  
High Fat Diet ◽  
Fat Body ◽  
Female Offspring ◽  
High Fat ◽  
Pregnant Rats ◽  
Glucose Levels ◽  
Thrifty Phenotype ◽  
Calorie Diet ◽  
Plasma Leptin

Maternal nutrient restriction results in intrauterine growth restriction (IUGR) newborns that develop obesity despite normal postweaning diet. The epidemic of metabolic syndrome is attributed to programmed “thrifty phenotype” and exposure to Western diets. We hypothesized that programmed IUGR newborns would demonstrate greater susceptibility to obesity and metabolic abnormalities in response to high-fat diet. From day 10 to term gestation and lactation, control pregnant rats received ad libitum (AdLib) food, whereas study rats were 50% food restricted (FR). Cross-fostering techniques resulted in three offspring groups: control (AdLib/AdLib), FR during pregnancy (FR/AdLib), and FR during lactation (AdLib/FR). At 3 weeks, offspring were weaned to laboratory chow or high-fat calorie diet (9% vs. 17% calorie as fat). Body composition, appetite hormones, and glucose and lipid profiles were determined in 9-mo-old male and female offspring. High-fat diet had no effect on body weight of AdLib/AdLib, but significantly increased weights of FR/AdLib and AdLib/FR offspring. High-fat diet significantly increased body fat, reduced lean body mass, and accentuated plasma leptin but not ghrelin levels in both sexes in all groups. In males, high-fat diet caused a significant increase in glucose levels in all three groups with increased insulin levels in AdLib/AdLib and AdLib/FR, but not in FR/AdLib. In females, high-fat diet had no effect on glucose but significantly increased basal insulin among all three groups. High-fat diet caused hypertriglyceridemia in all three groups although only food-restricted females exhibited hypercholesterolemia. Sex and offspring phenotype-associated effects of high-fat diet indicate differing pathophysiologic mechanisms that require specific therapeutic approaches.

scholarly journals Strawberry modulates inflammatory markers and insulin response to high fat meal in overweight men and women

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Collin Ellis ◽  
Mandeep Cheema ◽  
Amanda Linares ◽  
Dianne Hyson ◽  
Tissa Kappagoda ◽  
...  
Keyword(s):  
Inflammatory Markers ◽  
Insulin Response ◽  
High Fat ◽  
Men And Women ◽  
Fat Meal

scholarly journals Diurnal trends in responses of blood plasma concentrations of glucose, insulin, and C-peptide following high- and low-fat meals and their relation to fat metabolism in healthy middle-aged volunteers

1997 ◽  
Vol 77 (4) ◽  
pp. 523-535 ◽  
Author(s):  
David L. Frape ◽  
Norman R. Williams ◽  
A. J. Scriven ◽  
Christopher R. Palmer ◽  
Kathryn O'Sullivan ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Fat Metabolism ◽  
Plasma Concentrations ◽  
Insulin Response ◽  
Latin Squares ◽  
Postprandial Blood Glucose ◽  
High Fat ◽  
Middle Aged ◽  
C Peptide ◽  
Fat Meal

An experiment was conducted in twelve healthy middle-aged volunteers, six of each sex, with a mean BMI of 27kg/m2 to detect differences between morning and afternoon in postprandial blood glucose, insulin and C-peptide concentrations. These responses were measured following the consumption of isoenergetic meals that were high or low in fat content, at breakfast and at lunch. Over 4d each subject received the high-carbohydrate (L, 5·5 g mixed fat/meal) and moderately high-fat (M, 33 g mixed fat/meal) breakfasts and lunches, in three combinations (LL, MM, LM), or they fasted at breakfast time and received a moderately high-fat lunch (NM), in three Latin squares. Each evening a standard meal was given. Plasma glucose, insulin and C-peptide responses were greater following L than M meals and within both MM and LL treatments insulin and C-peptide responses were greater following breakfast than following lunch. The incremental C-peptide response to a fatty lunch following a fast at breakfast time (NM) was similar to that to a fatty breakfast, but the incremental insulin response for the same comparison was marginally lower at lunch (P=0·06). The relationship of C-peptide and insulin concentrations was assessed. Plasma glucose response to a fatty lunch was increased by a fatty breakfast. The relationships of these metabolic events with fat metabolism are discussed.

scholarly journals Potential Benefits on Impairment of Endothelial Function after a High-Fat Meal of 4 Weeks of Flavonoid Supplementation

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
T. A. Barringer ◽  
L. Hatcher ◽  
H. C. Sasser
Keyword(s):  
Endothelial Function ◽  
Statistical Significance ◽  
Reactive Hyperemia ◽  
Treatment Phase ◽  
High Fat ◽  
Peripheral Arterial Tonometry ◽  
Double Blind ◽  
The Difference ◽  
Peripheral Arterial ◽  
Fat Meal

Studies with foods high in flavonoids have demonstrated improvement in endothelial function. We investigated whether 4 weeks of flavonoid supplementation would prevent an adverse impact on endothelial function of a high-fat meal. Endothelial function was measured by reactive hyperemia peripheral arterial tonometry (RH-PAT). The RH-PAT index was measured both before and 3 h after a high-fat meal, in 23 healthy volunteers. Subjects were randomized in a double-blind, cross-over design to 4 weeks of daily supplementation with OPC-3, or a matching placebo. RH-PAT index before and after the high-fat meal was measured at the beginning and end of each 4-week treatment phase. The high-fat meal caused a decline in endothelial function at baseline in the placebo (-10.71%,P= .006) and flavonoid [-9.97% (P= .077)] groups, and there was no difference in decline between arms (P= .906). The high-fat meal produced a decline after 4 weeks of placebo [-12.37% (P= .005)], but no decline after 4 weeks of flavonoid supplement [-3.16% (P= .663)], and the difference between the two responses was highly significant (P< .0001). Within-group comparisons revealed no difference in endothelial function decline in the placebo arm between baseline and 4 weeks [-10.71% versus -12.37% (P= .758)]. In the flavonoid supplement arm, the difference in endothelial function decline between baseline and 4 weeks was -9.97% versus -3.16%, but did not reach statistical significance (P= .451). These results suggest that the flavonoid supplement used in this study mitigates the impairment of endothelial function caused by a high-fat meal. Whether certain subpopulations derive greater or lesser benefit remains unclear.

scholarly journals Differential effect of inbred mouse strain (C57BL/6, DBA/2, 129T2) on insulin secretory function in response to a high fat diet

2005 ◽  
Vol 187 (1) ◽  
pp. 45-53 ◽  
Author(s):  
Sofianos Andrikopoulos ◽  
Christine M Massa ◽  
Kathryn Aston-Mourney ◽  
Alexandra Funkat ◽  
Barbara C Fam ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
The Other ◽  
Mouse Strains ◽  
Secretory Function ◽  
High Fat ◽  
Glucose Levels ◽  
Fasting Plasma ◽  
First Phase Insulin Secretion

The increasing production of genetically-modified mouse models has necessitated studies to determine the inherent physiological characteristics of commonly used mouse strains. In this study we examined insulin secretory function in response to an intravenous bolus of glucose or glucose plus arginine in anesthetized C57BL/6, DBA/2 and 129T2 mice fed either a control or high fat diet for 6 weeks. The results show that 129T2 mice had higher fasting plasma glucose levels and lower fasting plasma insulin levels compared with C57BL/6 and DBA/2 mice regardless of diet. Furthermore, 129T2 mice were glucose intolerant and secreted significantly less insulin in response to glucose and glucose plus arginine irrespective of diet compared with the other two strains of mice. DBA/2 mice hypersecreted insulin in response to glucose and glucose plus arginine compared with C57BL/6 and 129T2 mice. Moreover while first phase insulin secretion was appropriately increased in response to the high fat diet in C57BL/6 and 129T2 mice, this was not the case for DBA/2 mice. Mean islet area was decreased in response to a high fat diet in DBA/2 mice, while there was no dietary effect on the other two strains. This study highlights the inherent genetic differences that exist among seemingly normal strains of mice that are commonly used to make transgenic and knockout mice. Understanding these differences will provide researchers with the information to choose the appropriate genetic background on which to express their particular genetic alteration.

scholarly journals The augmenting effect on insulin secretion by oral versus intravenous glucose is exaggerated by high-fat diet in mice

2008 ◽  
Vol 197 (1) ◽  
pp. 181-187 ◽  
Author(s):  
Bo Ahrén ◽  
Maria Sörhede Winzell ◽  
Giovanni Pacini
Keyword(s):  
Insulin Secretion ◽  
High Fat Diet ◽  
Insulin Response ◽  
Area Under The Curve ◽  
Oral Glucose ◽  
Incretin Effect ◽  
High Fat ◽  
Intravenous Glucose ◽  
Insulin Resistant ◽  
Glucose Levels

To study whether the incretin effect is involved in adaptively increased insulin secretion in insulin resistance, glucose was infused at a variable rate to match glucose levels after oral glucose (25 mg) in normal anesthetized C57BL/6J female mice or in mice rendered insulin resistant by 8 weeks of high-fat feeding. Insulin response was markedly higher after oral than i.v. glucose in both groups, and this augmentation was even higher in high-fat fed than normal mice. In normal mice, the area under the curve (AUCinsulin) was augmented from 4.0±0.8 to 8.0±1.8 nmol/l×60 min by the oral glucose, i.e. by a factor of 2 (P=0.023), whereas in the high-fat fed mice, AUCinsulin was augmented from 0.70±0.4 to 12.4±2.5 nmol/l×60 min, i.e. by a factor of 17 (P<0.001). To examine whether the incretin hormone glucagon-like peptide-1 (GLP-1) is responsible for this difference, the effect of i.v. GLP-1 was compared in normal and high-fat fed mice. The sensitivity to i.v. GLP-1 in stimulating insulin secretion was increased in the high-fat diet fed mice: the lowest effective dose of GLP-1 was 650 pmol/kg in normal mice and 13 pmol/kg in the high-fat diet fed mice. We conclude that 1) the incretin effect contributes by ∼50% to insulin secretion by the oral glucose in normal mice, 2) this effect is markedly exaggerated in insulin-resistant mice fed a high-fat diet, and 3) this augmented incretin contribution in the high-fat fed mice may partially be explained by GLP-1.

scholarly journals The effect of energy source and feeding level on the hormones of the entero-insular axis and plasma glucose in the growing pig

1991 ◽  
Vol 66 (2) ◽  
pp. 187-197 ◽  
Author(s):  
A. A. Ponter ◽  
D. N. Salter ◽  
L. M. Morgan ◽  
P. R. Flatt
Keyword(s):  
Small Intestine ◽  
Plasma Glucose ◽  
High Fat Diet ◽  
Plasma Insulin ◽  
Live Weight ◽  
High Fat ◽  
Feeding Level ◽  
Glucose Levels ◽  
Acute Test ◽  
Fat Meal

The aim of the experiment was to test the theory that accustoming pigs to a high-fat diet causes exaggerated gastric inhibitory polypeptide (GIP) secretion in response to a high-fat meal, and to determine whether hypersecretion of GIP could be related to an increase in the GIP content of the small intestine. Twenty-four pigs were fed one of three dietary regimens for 11 weeks: a high-carbohydrate diet (CL), or a high-fat diet (FL), both fed at 1.46 MJ gross energy (GE)/kg live weight0.75 per d, or a high-fat diet (FH) fed at 2.10 MJ GE/kg live weight0.75 per d. At the end of the period two acute tests were performed. For acute test 1 the accustomed meal (diets CL FL and FH) and for acute test 2 a standard high-fat meal (diet FL) were given; blood samples were taken during the next 5 h and analysed for GIP, insulin and glucose. Integrated increases in hormone and glucose levels were compared by analysis of variance (0–300 min). In acute test 1 there were significantly different plasma GIP concentrations between groups (CL > FH > FL; P < 0.05). Plasma insulin concentrations were significantly higher in group CL compared with groups FL and FH (P < 0.002). There were no differences in glucose levels. In acute test 2 integrated increases in plasma GIP (0–300 min) concentrations were not significantly different; however, GIP (0–45 min) concentrations were significantly higher in group FH than in groups CL and FL (P < 0.05). There were no differences in plasma insulin concentrations. Plasma glucose (0–300 min) concentrations were significantly higher in groups FL and FH compared with group CL (P < 0.05). The GIP content of tissue samples taken at the end of the experiment from the duodenum, jejunum, upper and lower ileum decreased significantly in a proximal to distal direction (P < 0.001). Diet FH significantly increased the average GIP content of the small intestine compared with diets CL and FL (P < 0.05). It is concluded that fat meal-stimulated GIP secretion was enhanced by increased feeding level during a pre-treatment phase, possibly due to an increase in GIP synthesis in the small intestine. The high-fat diet caused glucose intolerance after a high-fat meal. This may be due in part to the action of dietary fat on glucose transport and metabolism.

scholarly journals A Lipoprotein Lipase–Promoting Agent, NO-1886, Improves Glucose and Lipid Metabolism in High Fat, High Sucrose–Fed New Zealand White Rabbits

2003 ◽  
Vol 4 (1) ◽  
pp. 27-34 ◽  
Author(s):  
Weidong Yin ◽  
Zhonghua Yuan ◽  
Kazuhiko Tsutsumi ◽  
Yuxiang Xie ◽  
Qiuju Zhang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Insulin Response ◽  
Plasma Triglyceride ◽  
Acute Insulin Response ◽  
High Fat ◽  
Glucose Loading ◽  
Glucose Levels ◽  
Sucrose Diet ◽  
High Sucrose Diet ◽  
High Sucrose

The synthetic compound NO-1886 is a lipoprotein lipase activator that lowers plasma triglycerides and elevates high-density lipoprotein cholesterol (HDL-C). Recently, the authors found that NO-1886 also had an action of reducing plasma glucose in high-fat/high-sucrose diet–induced diabetic rabbits. In the current study, we investigated the effects of NO-1886 on insulin resistance andβ-cell function in rabbits. Our results showed that high-fat/high-sucrose feeding increased plasma triglyceride, free fatty acid (FFA), and glucose levels and decreased HDL-C level. This diet also induced insulin resistance and impairment of acute insulin response to glucose loading. Supplementing 1% NO-1886 into the high-fat/high-sucrose diet resulted in decreased plasma triglyceride, FFA, and glucose levels and increased HDL-C level. The authors also found a clear increased glucose clearance and a protected acute insulin response to intravenous glucose loading by NO-1886 supplementation. These data suggest that NO-1886 suppresses the elevation of blood glucose in rabbits induced by feeding a high-fat/high-sucrose diet, probably through controlling lipid metabolism and improving insulin resistance.

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