The role of n-3 long chain polyunsaturated fatty acids (LC n-3 PUFA) in reducing the risk of type 2 diabetes (T2DM) is not well established. The synthesis of LC n-3 PUFA requires fatty acid desaturase enzymes, which are encoded by the FADS gene. It is unclear if FADS polymorphism and dietary fatty acid intake can influence plasma or erythrocyte membrane fatty acid profile and thereby the risk of T2DM. Thus, the aim of this systematic review was to assess the current evidence for an effect of FADS polymorphism on T2DM risk and understand its associations with serum/erythrocyte and dietary LC n-3 PUFA. A systematic search was performed using PubMed, Embase, Cochrane and Scopus databases. A total of five studies met the inclusion criteria and were included in the present review. This review identified that FADS polymorphism may alter plasma fatty acid composition and play a protective role in the development of T2DM. Serum and erythrocyte LC n-3 PUFA levels were not associated with risk of T2DM, while dietary intake of LC n-3 PUFA was associated with lower risk of T2DM in one study only. The effect of LC n-3 PUFA consumption on associations between FADS polymorphism and T2DM warrants further investigation.

The fat type consumed is considered a risk factor for developing obesity and type 2 diabetes (T2D). However, these associations have not been investigated using a dietary patterns approach, which can capture combinations of foods and fat type consumed. This study aimed to investigate associations between dietary patterns with varying proportions of SFAs, MUFAs, or PUFAs and obesity, abdominal obesity, and self-reported T2D incidence. This study included UK Biobank participants with 2 or more 24-h dietary assessments, free from the outcome of interest at recruitment, and with outcome data at follow-up (n = 16,523; mean follow-up: 6.3 y). Reduced rank regression was used to derive dietary patterns with SFAs, MUFAs, and PUFAs (% of energy intake) as response variables. Logistic regression, adjusted for sociodemographic and health characteristics, was used to investigate the associations between dietary patterns and obesity [BMI (kg/m²) ≥30], abdominal obesity (waist circumference; men: ≥102 cm; women: ≥88 cm) and T2D incidence. Two dietary patterns, DP1 and DP2, were identified: DP1 positively correlated with SFAs (r = 0.48), MUFAs (r = 0.67), and PUFAs (r = 0.56), characterized by higher intake of nuts, seeds, and butter and lower intake of fruit and low-fat yogurt; DP2 positively correlated with SFAs (r = 0.76) and negatively with PUFAs (r = −0.64) and MUFAs (r = −0.01), characterized by higher intake of butter and high-fat cheese and lower intake of nuts and seeds. Only DP2 was associated with higher obesity and abdominal obesity incidence (OR: 1.24; 95% CI: 1.02, 1.45; and OR: 1.19; 95% CI: 1.02, 1.38, respectively). Neither of the dietary patterns was associated with T2D incidence. These findings provide evidence that a dietary pattern characterized by higher SFA and lower PUFA foods is associated with obesity and abdominal obesity incidence, but not T2D.

There is increasing evidence that skeletal muscle microvascular (capillary) blood flow plays an important role in glucose metabolism by increasing the delivery of glucose and insulin to the myocytes. This process is impaired in insulin-resistant individuals. Studies suggest that in diet-induced insulin-resistant rodents, insulin-mediated skeletal muscle microvascular blood flow is impaired post-short-term high fat feeding, and this occurs before the development of myocyte or whole-body insulin resistance. These data suggest that impaired skeletal muscle microvascular blood flow is an early vascular step before the onset of insulin resistance. However, evidence of this is still lacking in humans. In this review, we summarise what is known about short-term high-calorie and/or high-fat feeding in humans. We also explore selected animal studies to identify potential mechanisms. We discuss future directions aimed at better understanding the ‘early’ vascular mechanisms that lead to insulin resistance as this will provide the opportunity for much earlier screening and timing of intervention to assist in preventing type 2 diabetes.

Background: Although the impact of dietary fats on cardiovascular disease (CVD) risk is widely researched, longitudinal associations between dietary patterns (DPs) based on fat type and early markers of CVD risk remain unclear. Methods and Results: UK Biobank participants (46.9% men, mean age 55 years) with data on early markers of CVD risk (n=12 706) were followed longitudinally (2014–2020; mean 8.4 years). Two DPs (DP1, DP2) were derived using reduced rank regression (response variables: monounsaturated fat, polyunsaturated fat, and saturated fat based on two 24‐hour dietary assessments. Multivariable logistic and linear regression were used to investigate associations between DPs and odds of elevated CVD risk (using the nonlaboratory Framingham Risk Score) and changes in early CVD markers, respectively. DP1 (characterized by higher nuts and seeds and lower fruit and legumes intake) was positively correlated with saturated fat, monounsaturated fat, and polyunsaturated fat; DP2 (characterized by higher butter and high‐fat cheese, lower nuts and seeds intake) was positively correlated with saturated fat and negatively with polyunsaturated fat and monounsaturated fat. DP2 was associated with slightly higher odds of elevated CVD risk (odds ratio, 1.04 [95% CI, 1.00–1.07]). DP1 was associated with higher diastolic blood pressure (β, 0.20 [95% CI, 0.01–0.37]) and lower cardiac index (β, −0.02 [95% CI, −0.04 to −0.01]); DP2 was associated with higher carotid intima medial thickness (β, 1.80 [95% CI, 0.01–3.59]) and lower left ventricular ejection fraction (β, −0.15 [95% CI, −0.24 to −0.07]) and cardiac index (β, −0.01 [95% CI, −0.02 to −0.01]). Conclusions: This study suggests small but statistically significant associations between DPs based on fat type and some early markers of CVD risk. Further research is needed to confirm these associations.