The prevalence of overweight and obesity has grown at an alarming rate1, and sedentary lifestyle and inadequate dietary patterns, with high fat and sugar intake contribute to the positive energy balance. ^{1 , 2} In addition, excessive fat accumulation, mainly in the abdominal region, has been implicated in the development of other chronic noncommunicable diseases (CNCD), such as diabetes (DM), dyslipidemias, systemic arterial hypertension and cardiovascular diseases (CVD). ³

In this context, fatty acids are important components of diet that may influence the development of CVD, since fatty acids participate in important biological functions, such as energy substrate, regulation of metabolic pathways and inflammatory processes, hormone production, and participate in complex systems of intracellular signaling. Derivatives of fatty acids also act on the synthesis of prostaglandins, leukotrienes and thromboxanes, ^{4 , 5} being dietary fat important modulator of inflammatory status and cardiovascular risk. ⁶

The medium chain fatty acids are absorbed in the non-esterified form and transported to the liver, bound to albumin, where they are rapidly metabolized. In turn, long-chain fatty acids undergo a process of esterification, forming triglycerides, which can remain in the bloodstream, carried by chylomicrons, or released into the tissues, acting as a form of fat storage in the body. Thus, excessive deposition of these lipids may lead to an increase in CVD. ⁷ However, little is known about the relationship between the consumption of medium and long chain fatty acids and cardiovascular risk parameters.

Dietary fatty acids can also be classified as saturated (SFA), monounsaturated (MUFA), and polyunsaturated (PUFA), according to saturation level. In this sense, high MUFA diet causes reduction in serum levels of total cholesterol, low density lipoprotein (LDL-c), triglycerides and increase in high density lipoprotein (HDL-c). ^{8 , 9} The PUFAs, especially those of the omega 3 series, are recognized by cardioprotective activity. However, SFAs are associated with proven deleterious effects, since they increase triglyceridemia and cholesterolemia, and have a proinflammatory action. ¹⁰ Regarding inflammation modulation by fat, Studies have found strong association of saturated fat intake with the synthesis of inflammatory biomarkers compared to polyunsaturated fatty acids. ^{11 , 12}

In this sense, the objective of the present study was to verify the relationship between dietary fatty acids and cardiometabolic markers in individuals at cardiometabolic risk treated at the Cardiovascular Assistance Program of the Federal University of Viçosa (PROCARDIO-UFV).

Of the 282 subjects, 58.9% were female; 81.9% adults; 53.4% individuals reported practicing physical activity (self report) and 17.4% had diabetes. Of the overweight individuals, 76.6% were dyslipidemic (p = 0.028) ( Table 1 ).

Table 1

Variables n (%)	Total (n = 282)	Normal-weight (n = 85)	Overweight (n = 197)	p-values
Sex
Male	116 (41.1)	33 (38.8)	83 (42.1)	0.604
Female	166 (58.9)	52 (61.2)	114 (57.9)
Age
Adults	231 (81.9)	64 (75.3)	167 (84.8)	0.058
Seniors	51 (18.1)	21 (24.7)	30 (15.2)
Schooling (n = 265)
Illiterate incomplete/high school	62 (23.4)	17 (21.5)	45 (24.2)	0.479
Complete high school	46 (17.4)	11 (13.9)	35 (18.8)
Graduated/incomplete graduated	157 (59.2)	51 (64.6)	106 (57.0)
Income
Did not inform	30 (10.6)	12 (14.1)	18 (9.1)	0.399
Up to 2 wages	66 (23.4)	19 (22.4)	47 (23.9)
2 to 4 salaries	103 (36.5)	25 (29.4)	78 (39.6)
4 to 10 salaries	71 (25.2)	25 (29.4)	46 (23.4)
More than 10 wages	12 (4.3)	4 (4.7)	8 (4.1)
Smoking (n = 281)
Never smoked	189 (67.3)	65 (77.4)	124 (62.9)	0.014
Have you smoked	80 (28.5)	14 (16.7)	66 (33.5)
Smokes currently	12 (4.2)	5 (6)	7 (3.6)
Physical activity (n = 281)
No	131 (46.6)	42 (49.4)	89 (45.4)	0.537
Yes	150 (53.4)	43 (50.6)	107 (54.6)
Alcohol drink (n = 277)
Never drinks	114 (41.2)	34 (41)	80 (41.2)	0.648
Eventually	156 (56.3)	48 (57.8)	108 (55.7)
Daily	7 (2.5)	1 (1.2)	6 (3.1)
Hypertension (n = 281)
No	173 (61.6)	67 (79.8)	106 (53.8)	< 0.001
Yes	108 (38.4)	17 (20.2)	91 (46.2)
Diabetes (n = 281)
No	232 (82.6)	67 (79.8)	165 (83.8)	0.419
Yes	49 (17.4)	17 (20.2)	32 (16.2)
Dyslipidemia (n = 281)
No	56 (19.9)	10 (11.9)	46 (23.4)	0.028
Yes	225 (80.1)	74 (88.1)	151 (76.6)

Variables expressed as absolute and relative frequency. P values in bold refer to statistical significance (p <0.05) using the Pearson chi-square test. *Variables self-reported by participants.

Table 2 shows dietary fat intake according to weight-status. Among the overweight individuals, 45.7% presented fat intake within the recommendation, but 79.7% of individuals consumed above recommendation to SFA.

Table 2

Fat intake	Normal-weight (n = 85)	Overweight (n = 197)	p-values
Total fat
< 25 % CI (n = 93)	37 (43.5)	57 (28.9)	0.011
25% -35% CI (n = 127)	38 (44.7)	90 (45.7)
> 35% CI (n = 60)	10 (11.8)	50 (25.4)
Saturated fatty acid
≤ 7% CI (n = 68)	29 (34.1)	40 (20.3)	0.013
> 7% CI (n = 212)	56 (65.9)	157 (79.7)
Polyunsaturated fatty acid
≤ 10% CI (n = 252)	82 (96.5)	172 (87.3)	0.018
> 10% CI (n = 28)	3 (3.5)	25 (12.7)
Monounsaturated fatty acid
≤ 20% CI (n = 275)	84 (98.8)	193 (98.0)	0.618
> 20% CI (n = 5)	1 (1.2)	4 (2.0)

Variables expressed as absolute and relative frequency. p values in bold refer to statistical significance (p < 0.05) using the Pearson chi-square test. CI: caloric intake.

The individuals (normal-weight and overweight) with higher consumption of medium chain fatty acids had lower values (p < 0.05) for BMI, perimeters of the waist, hip waist ratios, waist height ratios, ferritin, glycemia and uric acid. On the other hand, they had higher values (p < 0.05) of total leukocytes, total cholesterol, low density lipoprotein (LDL), HDL and CRP ( Table 3 ). However, for long-chain fatty acids, only the total leukocyte count was significant (p = 0.038) for those with higher consumption (≥ 18.92 g/day) (data not shown). Individuals with higher intakes of palmitoleic acid presented higher values for BMI, body fat (%) and HOMA-IR ( Figure 1 ).

Table 3

Variável	Lower intake (< 1,05g/day)	Higher intake (≥ 1,05 g/day)	p
BMI (kg/m 2 )	29.48 (5.1)	28.20 (5.7)	0.049
Waist circumference (cm)	99.51(13.6)	94.09 (14.9)	0.002
Waist-hip ratio	0.96 (0.09)	0.91 (0.09)	< 0.001
Waist-height ratio	0.60 (0.09)	0.58 (0.10)	0.026
Total body fat (%)	30.30 (6.7)	31.66 (9.1)	0.222
Leukocytes (mil/mm 3 )	6,000 (5,120 - 7,035)	6,500 (5,425 - 7,750)	0.035
Ferritin (µg/L)	113.2 (54.9 - 237.7)	66.95 (30.5 - 153.0)	0.012
Uric acid (mg/dL)	4.5 (3.7 - 6.0)	3.9 (3.1 - 4.7)	0.002
Glycemia (mg/dL)	96.0 (87.0 - 108.0)	88.0 (80.8 - 97.0)	< 0.001
HOMA-IR	2.0 (1.2 - 3.4)	2.2 (1.5 - 3.0)	0.900
TyG	4.8 (0.3)	4.8 (0.3)	0.113
Total cholesterol (mg/dL)	195.2 (40.6)	215.6 (42.8)	< 0.001
LDL (mg/dL)	118.4 (37.4)	130.8 (37.6)	0.010
HDL (mg/dL)	44.7 (12.9)	51.4 (15.6)	< 0.001
TC/ HDL	4.64 (1.46)	4.49 (1.43)	0.402
LDL/HDL	2.81 (1.18)	2.75 (1.07)	0.696
Triglycerides (mg/dL)	140.0 (104.0 - 226.0)	146.5 (92.0 - 227.8)	0.597
CRP (mg/dL)	1.3 (0.3 - 3.2)	2.9 (0.8 - 5.8)	0.008

Data presented in mean and standard deviation or median (p25-p75). Values of p by t-test or Mann-Whitney

Figure 1

In relation to PUFA intake, 91.8% of study participants (n = 259) consume less than 0.6% of the total calories in α-linolenic acid, and 60.3% (n = 170) consume less than 5% of total calories in linoleic fatty acid. No significant relation was found between the recommended intake of α-linolenic acid (0.6-1.2% of total calories) and linoleic acid (5-10% of total calories) and cardiometabolic markers, neither there is significant result regarding the consumption of trans fatty acids (data not show).

In this study, 45.7% and 87.3% of the individuals with overweight had consumption within the total fat and PUFA recommendations, respectively, and 79.7% above the recommendation for saturated fatty acids. This result shows the importance of dietary fat assessment regarding to its quality, since dietary fatty acid is more important determinant of cardiovascular risk than its total amount. ^{30 , 31}

In previous study, with adults aged 20 to 59 years and overweight prevalence of 76.79%, SFA intake remained within the established values. However, there was an inadequacy of the PUFA consumption being below the recommended level. ³² This difference in results can be explained by the fact that the authors used the recommendations of up to 7% of total calories in SFA and up to 10% of total calories in PUFA, in the study cited, 10% of total calories and 6 to 10%, respectively.

In the last decades, there have been medical and nutritional recommendations for the reduction of the consumption of SFA due to the action of these in the increase of the LDL-c in the increase of the risk of cardiovascular disease. ³³ However, different SFA may have different effects on the lipid profile and cardiovascular risk factors. ³⁴

When compared to carbohydrates, lauric fatty acid (C12: 0) is what increases the LDL-c and consequently TC. ³⁵ This may explain the fact that the individuals in the present study had a higher intake of saturated medium chain fatty acids (SCMA), among them lauric acid, with higher values of TC and LDL. Considering the high prevalence of dyslipidemic in this population (80.1%, n = 225), this finding may contribute to the prescription of diets, restricting foods containing higher amounts of these fatty acids, such as whole milk and its derivatives, coconut and their derivatives.

Lower values in the adiposity indexes (BMI, perimeters of the waist, hip waist ratios, waist height ratios) of the participants with the highest consumption of SCMA can be explained by the metabolism of the medium chain triglycerides. These are absorbed, mainly as free fatty acids, directly from the portal vein, thus reaching the liver faster than the long chain fatty acids. In the liver, oxidation is rapid because it does not need to be activated by coenzyme A, making it a good ketogenic substrate. ^{36 , 37} In clinical trials with men and women fed a diet containing medium chain triglycerides, mainly lauric acid, they achieved a reduction in body mass and abdominal fat, since these components are not easily incorporated into adipose tissue triglycerides. ^{38 - 40}

Inflammation is a prominent feature of many chronic diseases, high-fat and carbohydrate meals contribute to increased oxidative stress and inflammation. ⁴¹ A high-fat meal has been suggested to increase inflammation, although there is currently no consensus regarding the specific changes in many of the pro-inflammatory markers that are often evaluated after a high-fat diet. ⁴²

SFA can cause inflammation of adipose tissue by processes involving, among others, the “toll-like receptor” TLR-4, a sensor that binds to bacterial lipopolysaccharide (LPS). ⁴³ High fat diets, especially those rich in SFA, have been shown to increase LPS uptake in the intestine. ^{44 , 45} Evidence suggests that SFA and LPS share the same inflammatory signaling pathway as TLR4, thus promoting the expression of proinflammatory transcription factors such as nuclear kappa B and cyclooxygenase-2. ⁴²

The subjects with higher intake of medium chain fatty acids had a higher total leukocyte count. It has been demonstrated that CRP-us ⁴⁶ and leukocyte count ⁴⁷ can independently predict vascular risk in apparently healthy men and women, asymptomatic for cardiovascular risk factors. ⁴⁶

A study conducted by Raz et al., ⁴⁸ with 54 subjects with a BMI of 25 ± 0.9 kg/m ² , with a mean age of 41.7 ± 3.1 years, demonstrated a significant increase in CRP-us after a high-acid meal (51 g), it did not work when the meal was high in monounsaturated fatty acids.

We also found tha individuals with higher intakes of C16: 1 (≥ 0.94g/day) had higher values for BMI, fat percentage and HOMA-IR. Studies evaluating the palmitoleic MUFA intake and its relation with cardiometabolic markers have not been reported yet. However, some studies have pointed out that higher proportions of palmitoleic acid in blood or adipose tissue are consistently associated with chronic diseases outcomes, such as obesity, ^{49 , 50} hypertriglyceridemia, ⁵¹ hyperglycemia, ⁵² inflammation, ^{53 , 54} metabolic syndrome, ^{55 , 56} diabetes type 2, ⁵⁷ disease coronary heart disease, ⁵⁷ and heart failure. ⁵⁸ In obese individuals with significant weight loss, high palmitoleic acid in adipose tissue was associated with higher inability to maintain weight loss. ⁵⁰ Moreover, in 18-week nutrition intervention study, with sixteen metabolic syndrome patients, ⁵⁹ plasma palmitoleic acid was gradually increasing when participants fed related low-carbohydrate diet to high-carbohydrate diet (47 to 346 g/d).

The study has as its limitation the use of only a 24-hour recall that provides us with current and not habitual diet information, although this food survey has been extensively used in epidemiological studies to investigate food consumption relationship with chronic diseases. ⁶⁰

In this cross-sectional study, individuals with a higher intake of medium-chain SFA had lower values of indicators of adiposity, ferritin, uric acid, and fasting glucose, and higher leukocyte, CRP, CT, LDL, and HDL concentrations. While higher palmitoleic MUFA consumption was related to higher BMI, fat percentage and HOMA-IR values. Our results suggest the relevance of a detailed assessment of the dietary fatty acid profile in the high-risk cardiometabolic population, considering chain size and saturation.