scholarly journals Effect of dietary fat intake and genetic risk on glucose and insulin-related traits in Brazilian young adults

Author(s):  
Sooad Alsulami ◽  
Nathália Teixeira Cruvinel ◽  
Nara Rubia da Silva ◽  
Ana Carolina Antoneli ◽  
Julie A. Lovegrove ◽  
...  

Abstract Purpose The development of metabolic diseases such as type 2 diabetes (T2D) is closely linked to a complex interplay between genetic and dietary factors. The prevalence of abdominal obesity, hyperinsulinemia, dyslipidaemia, and high blood pressure among Brazilian adolescents is increasing and hence, early lifestyle interventions targeting these factors might be an effective strategy to prevent or slow the progression of T2D. Methods We aimed to assess the interaction between dietary and genetic factors on metabolic disease-related traits in 200 healthy Brazilian young adults. Dietary intake was assessed using 3-day food records. Ten metabolic disease-related single nucleotide polymorphisms (SNPs) were used to construct a metabolic-genetic risk score (metabolic-GRS). Results We found significant interactions between the metabolic-GRS and total fat intake on fasting insulin level (Pinteraction = 0.017), insulin-glucose ratio (Pinteraction = 0.010) and HOMA-B (Pinteraction = 0.002), respectively, in addition to a borderline GRS-fat intake interaction on HOMA-IR (Pinteraction = 0.051). Within the high-fat intake category [37.98 ± 3.39% of total energy intake (TEI)], individuals with ≥ 5 risk alleles had increased fasting insulin level (P = 0.021), insulin-glucose ratio (P = 0.010), HOMA-B (P = 0.001) and HOMA-IR (P = 0.053) than those with < 5 risk alleles. Conclusion Our study has demonstrated a novel GRS-fat intake interaction in young Brazilian adults, where individuals with higher genetic risk and fat intake had increased glucose and insulin-related traits than those with lower genetic risk. Large intervention and follow-up studies with an objective assessment of dietary factors are needed to confirm our findings.

Diabetes Care ◽  
2012 ◽  
Vol 35 (7) ◽  
pp. 1532-1537 ◽  
Author(s):  
P. Xun ◽  
K. Liu ◽  
W. Cao ◽  
S. Sidney ◽  
O. D. Williams ◽  
...  

2014 ◽  
Vol 79 (1) ◽  
pp. 210-215 ◽  
Author(s):  
Jae-Hong Ryoo ◽  
Sung Keun Park ◽  
Ju Young Jung

Author(s):  
Shaza Abdalla Elwali ◽  
Sulaf I Abdelaziz

Background: Thyroid dysfunction is an endocrine disorder with a recognized association with type 2 diabetes mellitus. Thyroid hormones have a remarkable effect on glucose metabolism and can cause insulin resistance (IR). This study was aimed at assessing the relationship between IR and thyroid dysfunction. Methods: This case–control study was conducted at the endocrinology outpatient clinics of Ibrahim Malik Hospital and Omdurman Military Hospital in Khartoum State, Sudan between May 2018 and January 2019. Fasting blood glucose (FBG), fasting insulin level, and thyroid function test (TFT) were measured for each candidate and IR was estimated using the HOMA-IR equation. Results: Thirty-one patients with thyroid dysfunction and fifty-seven control participants were enrolled. The highest mean FBG was found among cases (105.3 ± 15.7 mg/dl) compared to the controls (97 ± 12.1 mg/dl), but the difference was not statistically significant (P-value = 0.598). The mean fasting insulin level was 9.22 ± 4 IU/ml in the cases and 9.4 ± 4.2 IU/ml in controls, without a significant difference (P-value = 0.681). The highest HOMA-IR score was found among cases (2.4 ± 1.2). It was 2.4 ± 1.3 in hyperthyroidism, 2.3 ± 1.1 in hypothyroidism, and 2.4 ± 1.2 in controls, and the difference was insignificant (P-value = 0.859). IR was higher in the cases (58.1%) compared to the controls (52.6%) but again not statistically significant (P-value = 0.396). Among cases, IR was encountered in 61.9% and 50% of hyperthyroid and hypothyroid patients, respectively. Conclusion: Patients with thyroid dysfunction have some level of IR that was not statistically significant when compared with controls.


2020 ◽  
Vol 44 (1) ◽  
Author(s):  
Ahmed Fayed ◽  
Ahmed Soliman ◽  
Mohamed Badr ◽  
Mohamed Abdelmoniem ◽  
Hesham Drwesh ◽  
...  

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