Genetics of fat intake in the determination of body mass

2017 ◽  
Vol 30 (1) ◽  
pp. 106-117 ◽  
Author(s):  
Agata Chmurzynska ◽  
Monika A. Mlodzik

AbstractBody mass and fat intake are multifactorial traits that have genetic and environmental components. The gene with the greatest effect on body mass is FTO (fat mass and obesity-associated), but several studies have shown that the effect of FTO (and of other genes) on body mass can be modified by the intake of nutrients. The so-called gene–environment interactions may also be important for the effectiveness of weight-loss strategies. Food choices, and thus fat intake, depend to some extent on individual preferences. The most important biological component of food preference is taste, and the role of fat sensitivity in fat intake has recently been pointed out. Relatively few studies have analysed the genetic components of fat intake or fatty acid sensitivity in terms of their relation to obesity. It has been proposed that decreased oral fatty acid sensitivity leads to increased fat intake and thus increased body mass. One of the genes that affect fatty acid sensitivity is CD36 (cluster of differentiation 36). However, little is known so far about the genetic component of fat sensing. We performed a literature review to identify the state of knowledge regarding the genetics of fat intake and its relation to body-mass determination, and to identify the priorities for further investigations.

2020 ◽  
Vol 79 (OCE2) ◽  
Author(s):  
Agata Chmurzynska ◽  
Monika Młodzik-Czyżewska ◽  
Anna Malinowska ◽  
Grzegorz Galinski ◽  
Anna Radziejewska ◽  
...  

AbstractTaste perception is the main biological determinant of food choice. It has thus been hypothesized that fatty acid sensitivity may affect fat intake. The aim of this study was to examine the relationship between fatty acid sensitivity, frequency of consumption of high-fat products, polymorphism of genes encoding proteins involved in fat taste perception, and body mass.421 people aged 20–40 were enrolled in Poznań, Poland. Body composition was measured using a Bod Pod. The frequency of consumption of high-fat foods was analyzed using an application for mobile devices based on the ecological momentary assessment approach. Food intake was assessed with dietary records. Salad dressings with varying concentrations of canola oil (from 2.5% to 40.0%) were used as stimuli to test fatty acid sensitivity. The individuals were then divided into groups with higher and lower fatty acid sensitivity. Lower sensitivity means that individuals were able to distinguish samples when the oil concentration exceeded 20%. Genotyping of rs1761667 (CD36), rs1573611 (FFAR1), and rs17108973 (FFAR4) was performed using TaqMan probes.57% men and 61% women had higher sensitivity to fatty acids. Higher fatty acid sensitivity was associated with the GG genotype of CD36 (OR = 2.05, p < 0.05). People with different taste sensitivity did not differ in their frequency of consumption of high-fat foods or in their macronutrient intake. There was no association between body mass index (BMI) and fatty acid sensitivity, but people with BMI values below 25 more often ate high-fat products with favorable lipid profiles and less often ate meat high-fat products than subjects with BMI values over 25 (p < 0.001 and p < 0.05, respectively). There was no association between CD36 or FFAR4 genotype and fat intake or frequency of consumption of high-fat foods. People with the minor FFAR1 allele ate sweet high-fat products less often than major allele homozygotes (p < 0.05). Moreover, women ate high-fat products with favorable lipid profiles and sweet and savory high-fat products more frequently than men (p < 0.05, p < 0.001, and p < 0.01), but men ate meat high-fat products more frequently than women (p < 0.01).Concluding, fatty acid sensitivity is associated with polymorphism of the CD36 gene. The frequency of consumption of high-fat foods depends on sex, but not on fatty acid sensitivity, BMI, or CD36 variants.The project was financed by a National Science Centre award (decision number grant no. 2014/15/B/NZ9/02134).


2013 ◽  
Vol 305 (11) ◽  
pp. R1346-R1355 ◽  
Author(s):  
Christina S.-Y. Chen ◽  
Elias M. Bench ◽  
Timothy D. Allerton ◽  
Allyson L. Schreiber ◽  
Kenneth P. Arceneaux ◽  
...  

Differential sensing of dietary fat and fatty acids by the oral cavity is proposed to regulate the susceptibility to obesity. In the current experiments, animals that differ in their susceptibility to obesity were used to investigate the influence of the oral cavity on the preference for the polyunsaturated fatty acid, linoleic acid. In experiment 1, the preference for differing concentrations of linoleic acid was determined in obesity-prone Osborne-Mendel (OM) and obesity-resistant S5B/Pl (S5B) rats. The preference threshold for linoleic acid was lower in S5B rats, compared with OM rats. To determine whether differences in linoleic acid preference threshold were related to innate strain differences in the fatty acid receptors on the tongue, the expression of GPR120, GPR40, and CD36 on the circumvallate papillae were assessed in OM and S5B rats. Results indicated that the expression of CD36, GPR40, and GPR120 did not differ between these two strains. Numerous studies have examined the role of CD36 on fat intake; therefore, in experiment 3, RNA interference was used to decrease the expression of CD36 on the tongues of OM and S5B rats, and the effect of decreased CD36 expression on linoleic acid preference was determined. CD36 siRNA attenuated linoleic acid preference for the most preferred concentration in both OM and S5B rats. Overall, these data indicate that there are innate differences in the preference threshold for linoleic acid in obesity-prone and obesity-resistant rats. Experimentally reducing the expression of CD36 on the circumvallate papillae attenuated the preference for linoleic acid in both strains.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Cara Dooley ◽  
Alice Ryan

Abstract Objectives The aim of the study was to examine the role of dietary consumption of different types of fatty acids on metabolic risk factors and regional fat deposition in older men and women. We hypothesized that saturated fatty acid (SFA) intake, ratio of monounsaturated fatty acids (MUFA) to polyunsaturated fatty acids (PUFA), and total fat intake, as well as proportion of energy derived from fat, would be associated with markers of insulin resistance, hyperlipidemia, and ectopic fat. Methods Sedentary, obese (Body Mass Index: 29–48 kg/m2) adults (N = 20) aged 45–78 years underwent two-hour oral glucose tolerance test, blood draw, DXA scan, and CT scan of the abdomen and mid-thigh. Seven-day diet records were analyzed with NutritionistPro software and the USDA Foodapedia feature of the Supertracker program. Results Subjects had low fitness levels (VO2 max = 23.5 ±2.4 mL/kg/min) and high total body fat (43.5 ± 1.7%) with abdominal obesity (visceral adipose tissue area = 192.4 ± 18 cm2, subcutaneous abdominal adipose area = 465.4 ± 29 cm2) and intermuscular adipose tissue (IMAT) area in thigh (150.1 ± 17 cm2). The average macronutrient composition of the diet was high in fat (fat as a % of total kcal = 35.5) with SFA, MUFA, and PUFA were respectively represented as 33.0, 34.8, and 22.1% of total fat intake. The average MUFA to PUFA ratio was 1.66. There were no differences in fatty acid intake between subjects with normal glucose tolerance and impaired glucose tolerance subjects. The ratio of MUFA to PUFA was positively correlated with higher fasting glucose (r = 0.42, P = 0.06), glucose intolerance (r = 0.43, P = 0.06), and serum cholesterol (r = 0.48, P = 0.03). PUFA intake as a percentage of fat intake was associated with lower serum cholesterol (r = –0.44, P = 0.05). Associations between diet composition with body composition (abdominal fat, IMAT) were not found to be uniformly significant among a homogenous sample of obese, sedentary subjects with diets high in proportion of lipid. Conclusions Dietary fatty acid intake, specifically MUFA unbalanced by PUFA, was associated with glucose intolerance and increased serum cholesterol, and therefore may confer increased risk for diabetes among obese, sedentary individuals. Future investigation of food sources, or context of dietary lipids, could lead to individualized dietary recommendations to promote healthy eating habits and potentially alter metabolic risk. Funding Sources Supported by grant awards from the Department of Veteran's Affairs and the National Institute of Health.


2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Athraa Alaulddin Al-Jawadi ◽  
Lidwina Priliani ◽  
Sukma Oktavianthi ◽  
Clarissa A. Febinia ◽  
Mulianah Daya ◽  
...  

Abstract Objective Recent studies showed that genetic polymorphisms in the fat mass and obesity-associated gene (FTO) were associated with obesity and dietary intake. In this study of 71 adults in Jakarta, Indonesia, we investigated FTO rs1421085 association with body mass index (BMI), macronutrient intake, and fatty acid intake. The association was evaluated using linear regression analyses assuming co-dominant, dominant, recessive, over-dominant, and additive genetic models. Results Only individuals with the CC genotype had a considerably higher BMI (p < 0.001), which indicates a recessive genetic trait, but the incidence for this genotype is low (68 TT + TC vs. 3 CC). Individuals with the minor C allele had an estimated increase of fat intake by 3.45–4.06% across various genetic models (dominant: p < 0.010, over-dominant: p < 0.030, additive: p < 0.010). Subjects with TC/CC genotypes had increased dietary monounsaturated fatty acid (MUFA; 1.14%, p = 0.046) and saturated fatty acid (SAFA; 2.06%, p = 0.023) intakes, compared to those with the TT genotype. In conclusion, our study provided evidence for the association between FTO rs1421085 risk allele with higher BMI and individual preferences for consuming more fat, MUFA, and SAFA. This study highlights the important role of FTO gene in food preference, and its influence on body weight.


2008 ◽  
Vol 3 (1) ◽  
pp. 57-65 ◽  
Author(s):  
M. L. Wahlqvist ◽  
L. Kaijser ◽  
B. W. Lassers ◽  
H. Löw ◽  
L. A. Carlson

2010 ◽  
Vol 51 (7) ◽  
pp. 1871-1877 ◽  
Author(s):  
Christopher D. Green ◽  
Cansel G. Ozguden-Akkoc ◽  
Yun Wang ◽  
Donald B. Jump ◽  
L. Karl Olson

1987 ◽  
Vol 26 (01) ◽  
pp. 1-6 ◽  
Author(s):  
S. Selvaraj ◽  
M. R. Suresh ◽  
G. McLean ◽  
D. Willans ◽  
C. Turner ◽  
...  

The role of glycoconjugates in tumor cell differentiation has been well documented. We have examined the expression of the two anomers of the Thomsen-Friedenreich antigen on the surface of human, canine and murine tumor cell membranes both in vitro and in vivo. This has been accomplished through the synthesis of the disaccharide terminal residues in both a and ß configuration. Both entities were used to generate murine monoclonal antibodies which recognized the carbohydrate determinants. The determination of fine specificities of these antibodies was effected by means of cellular uptake, immunohistopathology and immunoscintigraphy. Examination of pathological specimens of human and canine tumor tissue indicated that the expressed antigen was in the β configuration. More than 89% of all human carcinomas tested expressed the antigen in the above anomeric form. The combination of synthetic antigens and monoclonal antibodies raised specifically against them provide us with invaluable tools for the study of tumor marker expression in humans and their respective animal tumor models.


1981 ◽  
Author(s):  
M Yamamoto ◽  
K Watanabe ◽  
Y Ando ◽  
H Iri ◽  
N Fujiyama ◽  
...  

It has been suggested that heparin caused potentiation of aggregation induced by ADP or epinephrine. The exact mechanism of heparin-induced platelet activation, however, remained unknown. In this paper, we have investigated the role of anti-thrombin III ( AT ) in heparin-induced platelet activation using purified AT and AT depleted plasma. When ADP or epinephrine was added to citrated PRP one minute after addition of heparin ( 1 u/ml, porcine intestinal mucosal heparin, Sigma Co. USA ), marked enhancement of platelet aggregation was observed, compared with the degree of aggregation in the absence of heparin. However, in platelet suspensions prepared in modified Tyrode’s solution, heparin exhibited no potentiating effect on platelet aggregation induced by epinephrine or ADP. Potentiation of epinephrine- or ADP-induced platelet aggregation by heparin was demonstrated when purified AT was added to platelet suspensions at a concentration of 20 μg/ml. AT depleted plasma, which was prepared by immunosorption using matrix-bound antibodies to AT, retained no AT, while determination of α1-antitrypsinα2- macroglobulin and fibrinogen in AT depleted plasma produced values which corresponded to those of the original plasma when dilution factor was taken into account. The activities of coagulation factors were also comparable to those of the original plasma. Heparin exhibited potentiating effect on ADP- or epinephrine-induced aggregation of platelets in original plasma, but no effect in AT depleted plasma. When purified AT was added back to AT depleted plasma at a concentration of 20 μg/ml, potentiation of platelet aggregation by heparin was clearly demonstrated.Our results suggest that effect of heparin on platelet aggregation is also mediated by anti-thrombin III.


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