scholarly journals A Single Day of Excessive Dietary Fat Intake Reduces Whole-Body Insulin Sensitivity: The Metabolic Consequence of Binge Eating

Nutrients ◽  
2017 ◽  
Vol 9 (8) ◽  
pp. 818 ◽  
Author(s):  
Siôn Parry ◽  
Rachel Woods ◽  
Leanne Hodson ◽  
Carl Hulston
2017 ◽  
Vol 117 (2) ◽  
pp. 230-236 ◽  
Author(s):  
Tao Huang ◽  
Terri Beaty ◽  
Ji Li ◽  
Huijuan Liu ◽  
Wei Zhao ◽  
...  

AbstractDietary fat intake is correlated with increased insulin resistance (IR). However, it is unknown whether gene–diet interaction modulates the association. This study estimated heritability of IR measures and the related genetic correlations with fat intake, and tested whether dietary fat intake modifies the genetic influence on type 2 diabetes (T2D)-related traits in Chinese child twins. We included 622 twins aged 7–15 years (n 311 pairs, 162 monozygotic (MZ), 149 dizygotic (DZ)) from south-eastern China. Dietary factors were measured using FFQ. Structural equation models were fit using Mx statistical package. The intra-class correlation coefficients for all traits related to T2D were higher for MZ twins than for DZ twins. Dietary fat and fasting serum insulin (additive genetic correlation (rA) 0·20; 95 % CI 0·08, 0·43), glucose (rA 0·12; 95 % CI 0·01, 0·40), homoeostasis model of assessment-insulin resistance (Homa-IR) (rA 0·22; 95 % CI 0·10, 0·50) and the quantitative insulin sensitivity check index (Quicki) (rA −0·22; 95 % CI −0·40, 0·04) showed strong genetic correlations. Heritabilities of dietary fat intake, fasting glucose and insulin were estimated to be 52, 70 and 70 %, respectively. More than 70 % of the phenotypic correlations between dietary fat and insulin, glucose, Homa-IR and the Quicki index appeared to be mediated by shared genetic influence. Dietary fat significantly modified additive genetic effects on these quantitative traits associated with T2D. Analysis of Chinese twins yielded high estimates of heritability of dietary fat intake and IR. Genetic factors appear to contribute to a high proportion of the variance for both insulin sensitivity and IR. Dietary fat intake modifies the genetic influence on blood levels of insulin and glucose, Homa-IR and the Quicki index.


2008 ◽  
Vol 33 (2) ◽  
pp. 239-245 ◽  
Author(s):  
Jennifer L. Kuk ◽  
Lance E. Davidson ◽  
Robert Hudson ◽  
Katherine Kilpatrick ◽  
Kinga Bacskai ◽  
...  

Whether dietary fat influences the interaction between liver fat, visceral adipose tissue (VAT), and metabolic risk is unclear. Thus, we sought to determine the independent associations between 1 and 10 d dietary fat intake, liver fat, and VAT on insulin sensitivity using a cross-sectional design. Liver fat score (LFS) was assessed by computed tomography and VAT by magnetic resonance imaging in 42 abdominally obese older men. Insulin sensitivity was measured by the hyperinsulinemic–euglycemic clamp technique. Diet composition was determined from self-recorded diet records for 1 and 10 d preceding the assessment of LFS. LFS was positively associated with the 10 d average fat and alcohol intake, but not with any 1 d average dietary variables. VAT (r = –0.36) and LFS (r = –0.32) were both negatively correlated with insulin sensitivity (p < 0.05). When LFS and VAT were entered in the same model, only VAT was an independent predictor of insulin sensitivity (p < 0.05). Control for the average 10 d alcohol consumption and fat intake improved the association between insulin sensitivity and LFS (from r = –0.32, p > 0.10 to r = –0.49, p < 0.05), but not VAT. In fact, after control for the 10 d dietary variables, both LFS and VAT were independent predictors of insulin sensitivity (p < 0.05). This was not true for any of the 1 d dietary intake variables. In conclusion, liver fat is associated with dietary fat intake and alcohol consumption over 10 d, but not 1 d. Furthermore, dietary habits may influence the relationship between liver fat and insulin sensitivity.


2018 ◽  
Vol 108 (5) ◽  
pp. 1129-1134 ◽  
Author(s):  
Tao Zhou ◽  
Dianjianyi Sun ◽  
Yoriko Heianza ◽  
Xiang Li ◽  
Catherine M Champagne ◽  
...  

ABSTRACT Background Obesity is closely associated with bone health. Although diet and weight loss produce many metabolic benefits, studies of weight loss diets on bone health are conflicting. Genetic variations, such as vitamin D levels, may partly account for these conflicting observations by regulating bone metabolism. Objective We investigated whether the genetic variation associated with vitamin D concentration affected changes in bone mineral density (BMD) in response to a weight-loss diet intervention. Design In the 2-y Preventing Overweight Using Novel Dietary Strategies (POUNDS Lost) trial, BMD was measured for 424 participants who were randomly assigned to 1 of 4 diets varying in macronutrient intakes. A genetic risk score (GRS) was calculated based on 3 genetic variants [i.e., 7-dehydrocholesterol reductase (DHCR7) rs12785878, cytochrome P450 2R1 (CYP2R1) rs10741657 and group-specific component globulin (GC) rs2282679] related to circulating vitamin D levels. A dual-energy X-ray absorptiometry scan was performed to assess changes in whole-body BMD over 2 y. The final analysis included 370 participants at baseline. Results We found a significant interaction between dietary fat intake and vitamin D GRS on 2-y changes in whole-body BMD (P-interaction = 0.02). In the high-fat diet group, participants with higher GRS showed significantly less reduction in whole-body BMD than those with lower GRS, whereas the genetic associations were not significant in the low-fat diet group. We also found a significant interaction between dietary fat intake and the GRS on 6-mo change in femur neck BMD (P-interaction = 0.02); however, the interaction became nonsignificant at 2 y. Conclusion Our data indicate that dietary fat intake may modify the effect of vitamin D–related genetic variation on changes in BMD. Overweight or obese patients predisposed to sufficient vitamin D may benefit more in maintaining BMD along with weight loss by eating a low-fat diet. This trial was registered at clinicaltrials.gov as NCT03258203.


Gut ◽  
2018 ◽  
Vol 68 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Yoriko Heianza ◽  
Dianjianyi Sun ◽  
Xiang Li ◽  
Joseph A DiDonato ◽  
George A Bray ◽  
...  

ObjectiveAlterations in gut microbiota have been linked to host insulin resistance, diabetes and impaired amino acid metabolism. We investigated whether changes in gut microbiota-dependent metabolite of trimethylamine N-oxide (TMAO) and its nutrient precursors (choline and L-carnitine) were associated with improvements in glucose metabolism and diabetes-related amino acids in a weight-loss diet intervention.DesignWe included 504 overweight and obese adults who were randomly assigned to one of four energy-reduced diets varying in macronutrient intake. The 6-month changes (Δ) in TMAO, choline and L-carnitine levels after the intervention were calculated.ResultsGreater decreases in choline and L-carnitine were significantly (p<0.05) associated with greater improvements in fasting insulin concentrations and homeostasis model assessment of insulin resistance (HOMA-IR) at 6 months. The reduction of choline was significantly related to 2-year improvements in glucose and insulin resistance. We found significant linkages between dietary fat intake and ΔTMAO for changes in fasting glucose, insulin and HOMA-IR (pinteraction <0.05); a greater increase in TMAO was related to lesser improvements in the outcomes among participants who consumed a high-fat diet. In addition, ΔL-carnitine and Δcholine were significantly related to changes in amino acids (including branched-chain and aromatic amino acids). Interestingly, the associations of ΔTMAO, Δcholine and ΔL-carnitine with diabetes-related traits were independent of the changes in amino acids.ConclusionOur findings underscore the importance of changes in TMAO, choline and L-carnitine in improving insulin sensitivity during a weight-loss intervention for obese patients. Dietary fat intake may modify the associations of TMAO with insulin sensitivity and glucose metabolism.Trial registration numberNCT00072995.


2013 ◽  
Author(s):  
Eleanor B. Tate ◽  
Susan M. Schembre ◽  
Gillian O'Reilly ◽  
Mary Ann Pentz ◽  
Genevieve Dunton

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1893-P
Author(s):  
AMBER B. COURVILLE ◽  
SHANNA BERNSTEIN ◽  
MIRELLA GALVAN-DE LA CRUZ ◽  
ANTHONY ONUZURUIKE ◽  
NIRUPA R. MATTHAN ◽  
...  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1734-P
Author(s):  
AUSTIN REILLY ◽  
SHIJUN YAN ◽  
ALEXA J. LONCHARICH ◽  
HONGXIA REN

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