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Adherence to the dietary approaches to stop hypertension (DASH) and risk of pancreatic steatosis

Abstract

Background

The Dietary Approach to Stop Hypertension (DASH) has shown positive effects on various health factors that may be related to pancreatic steatosis (PS). This study aimed to investigate the association between adherence to the DASH diet and the risk of developing PS.

Methods

This case-control study was conducted on 278 patients diagnosed with gallstone disease and referred to Taleghani Hospital (Tehran, Iran). Among the participants, 89 were diagnosed with PS based on an endoscopic ultrasound (EUS) examination, while 189 patients did not exhibit this condition. The dietary intake of patients was assessed using a validated food frequency questionnaire (FFQ). Participants were classified based on the DASH diet score. Multiple logistic regression models estimated crude and multivariable-adjusted odds ratios (ORs) and 95% confidence intervals (CIs).

Results

The mean ± SD of DASH score in PS patients and controls was 23.68 ± 4.38 and 25.27 ± 4.2, respectively (P = 0.006). The risk of PS in the highest tertile of DASH score was 64% lower than the lowest tertile (OR = 0.36, 95%CI: 0.17–0.75, P = 0.005) after full adjustment for confounders. Also, more intake of vegetables and whole grains and less intake of sodium, red and processed meat were each significantly associated with reduced risk of PS.

Conclusions

Our data prove that adherence to the DASH diet was associated with a lower risk of PS. Further prospective studies are warranted to confirm these associations and explore the underlying mechanisms.

Highlights

The findings of this study highlight the potential role of following the DASH diet in reducing the risk of developing PS.

Adherence to a DASH dietary pattern, emphasizing the consumption of “vegetables” and “whole grains” while limiting “red and processed meats” and “sodium”, may be associated with decreased odds of PS.

The present study provides the first evidence of an association between the DASH diet and PS odds.

Despite the relatively high prevalence of PS, the lack of specific treatment approaches and its association with pancreatic cancer, the role of nutrition in it has not been elucidated, and this knowledge gap is addressed in this study.

This study points to the potential role of dietary interventions in the prevention and management of PS.

Introduction

The concept of pancreatic steatosis (PS), which is characterized by the accumulation of fat in the pancreas, was first described by Ogilvie in 1933, who noted higher fat levels in the pancreas of obese individuals compared to non-obese individuals [1]. PS is an umbrella term that refers to the accumulation of fat in the pancreas and, when caused by obesity and metabolic syndrome, is known as non-alcoholic fatty pancreas disease (NAFPD) [2]. The prevalence of PS has been extensively studied in Asian populations, with reported rates ranging from 16 to 35% [3]. Likewise, a meta-analysis based on pooled data found an overall prevalence of 33% for NAFPD [4]. The association of PS with metabolic syndrome, type 2 diabetes mellitus, hypertension [5, 6], and obesity [5,6,7] has been demonstrated in previous studies. Furthermore, studies have demonstrated a direct correlation between fatty pancreas and pancreatic cancer [8, 9], which is a leading cause of cancer-related deaths globally [10]. Currently, no specific therapy is available for fatty pancreas, and the management of PS depends on treating its underlying causes [11]. It seems that adherence to a healthy diet, engaging in regular physical activity, reducing red meat consumption, and quitting smoking are beneficial in the amendment of PS [12].

Among various dietary patterns, the Dietary Approach to Stop Hypertension (DASH) has gained recognition as a popular and healthy diet over the past two decades [13, 14]. Initially developed to lower blood pressure [15], the DASH-style diet emphasizes increased consumption of fruits, vegetables, whole grains, and low-fat dairy products, while reducing the intake of red meat and sweets [16]. Adherence to the DASH diet lead to favorable effects on blood pressure [17], diabetes mellitus [18], insulin sensitivity [19], obesity [20], lipid profile [21], and cancers [22].

Given the relatively high prevalence of PS, the lack of specific treatment approaches, and its association with pancreatic cancer, managing PS is of utmost importance. On the other hand, compliance with the DASH diet has been found to have beneficial effects on the underlying factors contributing to PS. Therefore, our current study aimed to examine the association between adherence to the DASH diet and the risk of developing PS.

Material & methods

Study design and participants

This case-control study was done on 278 patients diagnosed with choledocholithiasis who were referred to Taleghani Hospital (Tehran, Iran). Among the participants, 89 were identified with PS based on an endoscopic ultrasound (EUS) examination (case group), while 189 patients did not exhibit this condition (control group). Enrollment in this study lasted from July 1, 2022 to the end of May 2023. The sample size for present case–control study was calculated using a significance level of 5%, Z1−α/2 = 1.96, 80% power, Z1−β = 0.84, odds ratio = 3. A minimum sample size of 80 subjects was calculated. Double this number was considered for the control group.

Pregnant and lactating women, as well as individuals with active malignancy, hepatitis, cirrhosis, and renal failure, were excluded from the sample. Each participant was assigned a code, while face-to-face interviews and measurements were conducted in a private room, and participants were assured of confidentiality. The written informed consent form was signed by all participants prior to enrollment. The Research Ethics Committees of Vice-Chancellor in Research Affairs of Shahid Beheshti University of Medical Sciences reviewed and approved the study methods and design (Ethics code: IR.SBMU.RETECH.REC.1402.689). Moreover, the latest version of the Helsinki Declaration was followed throughout the entire procedure.

Anthropometric measurements

The weight was measured using a digital scale with an accuracy of 0.1 kg. A wall-mounted caliper was used to measure height with an accuracy of 0.1 cm, and mid-arm span was measured for patients who were unable to stand. To calculate body mass index (BMI), weight (in kilograms) was divided by the square of height (in meters).

Dietary intake assessment

The dietary intake of patients was assessed using a validated food frequency questionnaire (FFQ) [23]. The frequency of consumption of each food item during the previous year was collected through individual interviews conducted by a skilled nutritionist. The initial step in the analysis involved converting the quantity of food consumed into grams, followed by the calculation of nutrient and energy values using the food composition table provided by the United States Department of Agriculture (USDA). Additionally, an Iranian food composition table was utilized to account for local food items and their respective nutritional information.

In this study, the calculation of the DASH score involved the evaluation of eight elements, namely “fruits”, “vegetables”, “legumes, nuts and seeds”, “whole grains”, “low-fat dairy”, “red and processed meats”, “sweetened beverages”, and “sodium”. Energy adjustments were conducted for every food component (g/1000). The dietary intake of these components was ranked in five quintiles. Scoring for low-fat dairy, fruits, vegetables, whole grains, legumes, nuts and seeds was based on consumption quintiles, that is, the lowest consumption (first quintile) was assigned the lowest score (1 point). Conversely, the scoring for red and processed meats, sugar-sweetened beverages, and sodium was reversed, i.e., the highest score (5 points) was given to the lowest quintile. Finally, based on the scores of these eight components, the DASH score was calculated. The calculation of DASH scores followed the procedure outlined by Fung et al. [24].

Statistical analysis

First, a histogram graphic and the Kolmogorov-Smirnov test were used to check the distribution of variables. The participants were divided into tertiles based on their DASH diet score cutoff points (≤ 22, 23–26, and ≥ 27). The participants’ baseline characteristics were given as the mean ± SD for continuous variables and the percentages for categorical variables across tertiles of the DASH score. Analysis of variance (ANOVA) was used to analyze the trend and P-value of continuous variables across the tertiles of the DASH score and χ2 test was applied for qualitative variables. Logistic regression analyses were also performed to estimate the OR and 95% CI of the occurrence of PS across tertiles, using the first tertile as the reference. Three models were employed to assess the correlation between the DASH scores and the odds of PS, while taking into account sex, age, BMI, and daily calorie intake as potential factors that could distort the results. The data analyses were conducted using SPSS software (version 26.0; SPSS Inc., Chicago, IL). A P-value of less than 0.05 was considered statistically significant.

Results

The basic characteristics of the study participants by tertiles of the DASH score are presented in Table 1. The table indicates that age, DASH score, and dietary intakes including energy, carbohydrate, protein, and fat differed significantly among the tertiles of DASH score, while BMI and sex did not vary significantly across the tertiles of DASH score. The study population consisted of 34% males and 66% females. The mean ± SD of age and BMI of patients was 55.74 ± 15.16 years and 27.63 ± 5.23 kg/m2, respectively. According to the medical record, 17 (6%) participants had diabetes, 26 (4.9%) had hypertension, and 15 (4.5%) had dyslipidemia. In terms of comorbidities, there was no difference between cases and controls.

Table 1 Basic characteristics of study participants based on DASH scores tertile

Table 2 shows the ORs (95% CIs) of the association between DASH components and the risk of PS. Higher “vegetable” consumption was significantly associated with a 59–79% lower risk of PS in all the models. Similarly, higher intake of “whole grains” also showed a significant association with a decreased risk (p < 0.001). However, “fruit,“, “legumes, nuts, and seeds,” as well as “low-fat dairy consumption,” did not demonstrate a significant association with PS risk. On the other hand, consuming “red and processed meats” was significantly associated with a 5.5–10.2 times increased risk (p < 0.001). Furthermore, although “sweet beverages” consumption did not show a significant association with PS risk in crude and model 1, after adjustment for further variables, the association became significant (OR: 2.96, 95% CI: 1.151–7.6) (p = 0.026). Higher sodium intake was also significantly associated with an elevated risk (OR: 5.7, 95% CI: 2.5–12.8). These associations were consistent across both Model 1 (OR: 5.7, 95%CI: 2.4–13.4) and Model 2 (OR: 10, 95%CI: 3.57–28.19) (p < 0.001, for all the models). Although in the crude model and the first model, moderate sodium consumption was associated with a slight decrease in the risk of PS, but after adjusting for other food groups, it was shown that more sodium intake has a significant relationship with an increase in the risk of PS.

Table 2 95% odds and confidence interval of the relationship between DASH score components with the risk of pancreatic steatosis

The odds ratio (95% CI) of PS risk by tertiles of DASH scores has been presented in Table 3. In Model 1 (Crude model) and Model 2 (adjusted for age and sex), being in the last tertiles of DASH scores was linked to 53% (OR T3 vs. T1: 0.47, 95% CI: 0.24–0.89) and 54% (OR T3 vs. T1: 0.46, 95%CI: 0.23–0.9) lower odds of PS. Besides, after additionally adjustment for BMI and energy intake, the last tertile of DASH scores was related to 64% lower odds of PS (OR T3 vs. T1: 0.36, 95%CI: 0.17–0.75).

Table 3 Odds ratio (95% CI) pancreatic steatosis risk according to tertiles of DASH scores

Dietary intakes of food groups are shown in Fig. 1 according to tertiles of DASH score. While a significant difference was observed for “vegetables,” “fruits,” “legumes, nuts, and seeds” and “seet beverages” across the tertiles of the DASH score, there was no significant disparity for other food groups.

Fig. 1
figure 1

Dietary intakes of food groups according to tertiles of DASH score. * Denotes significant difference, DASH: Dietary Approach to Stop Hypertension

Discussion

To the best of our knowledge, the present study is the first one to investigate the association between adherence to the DASH diet and the risk of PS. The results of our study indicated that the last tertile of DASH score was associated with 64% lower risk of PS. Additionally, further analysis was performed to examine the association of individual components of the DASH score and odds of PS, which showed that more intake of “vegetables” and “whole grains” and less intake of “red and processed meats” and “sodium” were linked to a lower risk of PS. Also, the association of “fruits”, “legumes”, “nuts and seeds”, “low-fat dairy” or “sweetened beverages” with the risk of PS was “U-shaped”, but not statistically significant. However, for sweetened beverages, the relationship was significant after adjusting for all confounders.

Although the underlying mechanism(s) of PS development are still poorly understood, a number of mechanisms [25] might explain our findings. It has been shown that individuals without a history of pancreatic disease can develop PS due to inappropriate diets that promote obesity [26]. Moreover, some experimental studies have shown the role of obesity and body fat in development of PS. An experimental study with 30 obese and 30 lean female mice showed that the obese mice had higher fat content, triglycerides, free fatty acids, cholesterol, and pro-inflammatory cytokines (IL-1β and TNFα) in their pancreas than the lean mice [27]. Obesity also reduces the expression of IL-10 in the spleen, which protects the pancreas from inflammation [28]. Maternal obesity and obesogenic diets in the postnatal period can also disrupt the circadian metabolic cycles or endoplasmic reticulum of offsprings, resulting in PS [29, 30]. In addition, it has been shown that increased PS is associated with increased expression of IL-6 and TNF-α, as the markers of inflammation in the body [30]. Thus, it seems that both obesity and inflammation are involved in pathogenesis of PS. On the other hand, it has been shown that DASH diet can prevent from both obesity, and inflammation. There is extensive evidence supporting the effectiveness of the DASH diet in promoting weight loss [31, 32], decreasing fat mass [33], and enhancing immune cell function [34]. Thus, adhering to a dietary regimen like DASH, which has beneficial impacts on obesity and inflammation, might greatly impact the pathophysiology of PS.

Another potential mechanism explaining our findings is associated with the components of the DASH diet. One of the DASH recommendation is reduction in consumption of saturated fat [35], especially from red meat, and processed meat, which was significantly correlated with PS in our study. A high-fat diet affects pancreatic physiology through a complex interplay of saturated and unsaturated fatty acids, as well as the total fat content [36]. Saturated fatty acids (SFAs) have a detrimental effect on beta-cell survival [37]. Besides, it has been shown that oleic acid (C18:1n-9) and palmitic acid (C16:0) are highly linked to the amount of triglycerides stored in the pancreas [38]. These findings underscore the importance of total and type of dietary fat.

Another component of DASH diet, which leads to amelioration of hypertension is reduction of sodium intake in this diet. An analysis of 55 pancreas donors who did not have diabetes revealed that individuals with hypertension exhibited a higher amount of fat in their pancreas and islet cells [39]. Indeed, hypertension can elevate pancreatic fat levels regardless of other risk factors. Hypertension impairs tissue perfusion by constricting small vessels and reducing microvascular density [40]. This makes hypoxia happen and turns on hypoxia-inducible factors, which change the lipids’ metabolism and cause them to build up in organs like the pancreas and liver [41, 42].

Other components of DASH, which were significantly related with PS risk, were high consumption of vegetable, and whole grains. Vegetables, and whole grains are rich in dietary fiber [43, 44], which can reduce BMI and body fat [45]. Vegetables are also known to contain antioxidants that can counteract the inflammation induced by obesity and fat accumulation [46]. Thus, it seems that high consumption of these groups of foods can reduce risk of PS by reduction in body fat, and inflammation.

In this study, there was no significant relationship between fruit consumption and PS. Moderate consumption of fruit showed a protective effect and high consumption of fruit showed promoting effects, although it was not statistically significant. The protective effect of the fruit can be attributed to its fiber content and antioxidants, which are associated with a reduced risk of PS risk factors such as metabolic syndrome and insulin resistance [5, 6]. While the fructose content of fruits in high consumption can lead to visceral obesity by increasing cortisol. The increase of free fatty acids and its entry into visceral organs such as the liver and pancreas can disrupt the metabolic processes and function of the organs and cause steatosis of the liver and pancreas [47].

This study is characterized by several notable strengths. The present study provides the first evidence of an association between the DASH diet and PS odds. A validated FFQ was used for dietary data collection. Both groups were recruited from the same center, which results in the same socioeconomic status. A specialist performed the diagnosis, and it was similar for both groups to control information bias. Besides, a trained dietician who was blinded to the diagnosis completed the interview. Nonetheless, there are several limitations to this study. Selection bias, measurement bias, and recall bias for FFQ may lead to misleading findings in a case-control study. Furthermore, it is important to note that alcohol and opium are considered taboos in our country, so no data was collected on these variables. Moreover, while we examined adjusted models to account for potential confounding factors, it is crucial to recognize the possibility of undiscovered confounding factors. Besides, although many confounding variables were considered, it was not possible to assess genetic factors and other potential factors. Finally, the study design limits the establishment of a causal relationship between the DASH score and PS, and the generalizability of the findings may be limited to the specific population studied.

Conclusion

In conclusion, this case-control study suggests that adherence to a DASH dietary pattern, emphasizing the consumption of “vegetables” and “whole grains” while limiting “red and processed meats” and “sodium”, may be associated with decreased odds of PS. These findings highlight the potential role of dietary interventions in the prevention and management of PS. Further prospective studies are warranted to confirm these associations and explore the underlying mechanisms.

Data availability

Datasets used and/or analyzed during this study can be obtained from the corresponding author upon reasonable request.

References

  1. Schaefer JH, THE NORMAL WEIGHT OF THE PANCREAS IN. THE ADULT HUMAN BEING: A BIOMETRIC STUDY ¹. Anat Rec. 1926;32(2):119.

    Article  Google Scholar 

  2. Smits MM, van Geenen EJ. The clinical significance of pancreatic steatosis. Nat Rev Gastroenterol Hepatol. 2011;8(3):169–77.

    Article  PubMed  Google Scholar 

  3. Yu TY, Wang CY. Impact of non-alcoholic fatty pancreas disease on glucose metabolism. J Diabetes Invest. 2017;8(6):735–47.

    Article  Google Scholar 

  4. Singh RG, Yoon HD, Wu LM, Lu J, Plank LD, Petrov MS. Ectopic fat accumulation in the pancreas and its clinical relevance: a systematic review, meta-analysis, and meta-regression. Metabolism. 2017;69:1–13.

    Article  CAS  PubMed  Google Scholar 

  5. Bi Y, Wang JL, Li ML, Zhou J, Sun XL. The association between pancreas steatosis and metabolic syndrome: a systematic review and meta-analysis. Diab/Metab Res Rev. 2019;35(5):e3142.

    Article  Google Scholar 

  6. Tirkes T, Jeon CY, Li L, Joon AY, Seltman TA, Sankar M, et al. Association of pancreatic steatosis with chronic pancreatitis, obesity, and type 2 diabetes Mellitus. Pancreas. 2019;48(3):420–6.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Rosso E, Casnedi S, Pessaux P, Oussoultzoglou E, Panaro F, Mahfud M, et al. The role of fatty pancreas and of BMI in the occurrence of pancreatic fistula after pancreaticoduodenectomy. J Gastrointest Surg. 2009;13:1845–51.

    Article  PubMed  Google Scholar 

  8. Rebours V, Gaujoux S, d’Assignies G, Sauvanet A, Ruszniewski P, Lévy P, et al. Obesity and fatty pancreatic infiltration are risk factors for pancreatic precancerous lesions (PanIN). Clin Cancer Res. 2015;21(15):3522–8.

    Article  CAS  PubMed  Google Scholar 

  9. Hori M, Takahashi M, Hiraoka N, Yamaji T, Mutoh M, Ishigamori R, et al. Association of pancreatic fatty infiltration with pancreatic ductal adenocarcinoma. Clin Translational Gastroenterol. 2014;5(3):e53.

    Article  CAS  Google Scholar 

  10. Ilic M, Ilic I. Epidemiology of pancreatic cancer. World J Gastroenterol. 2016;22(44):9694.

    Article  PubMed  PubMed Central  Google Scholar 

  11. Paul J, Shihaz AVH. Pancreatic steatosis: a new diagnosis and therapeutic challenge in gastroenterology. Arq Gastroenterol. 2020;57:216–20.

    Article  PubMed  Google Scholar 

  12. Ramkissoon R, Gardner TB. Pancreatic steatosis: an emerging clinical entity. Official J Am Coll Gastroenterology| ACG. 2019;114(11):1726–34.

    Article  Google Scholar 

  13. Fm S. Effects on blood pressure of reduced dietary sodium and the Dietary approaches to stop hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J Med. 2001;344:3–10.

    Article  Google Scholar 

  14. Svetkey LP, Sacks FM, Obarzanek E, Vollmer WM, Appel LJ, Lin P-H, et al. The DASH diet, sodium intake and blood pressure trial (DASH-sodium): rationale and design. J Am Diet Assoc. 1999;99(8):S96–104.

    Article  CAS  PubMed  Google Scholar 

  15. Vogt TM, Appel LJ, Obarzanek E, Moore TJ, Vollmer WM, Svetkey LP, et al. Dietary approaches to stop hypertension: rationale, design, and methods. J Am Diet Assoc. 1999;99(8):S12–8.

    Article  CAS  PubMed  Google Scholar 

  16. Nih N. Your guide to lowering your blood pressure with DASH. Blood. 2006;64.

  17. Filippou CD, Tsioufis CP, Thomopoulos CG, Mihas CC, Dimitriadis KS, Sotiropoulou LI, et al. Dietary approaches to stop hypertension (DASH) diet and blood pressure reduction in adults with and without hypertension: a systematic review and meta-analysis of randomized controlled trials. Adv Nutr. 2020;11(5):1150–60.

    Article  PubMed  PubMed Central  Google Scholar 

  18. Liese AD, Nichols M, Sun X, D’Agostino Jr RB, Haffner SM. Adherence to the DASH Diet is inversely associated with incidence of type 2 diabetes: the insulin resistance atherosclerosis study. Diabetes Care. 2009;32(8):1434–6.

    Article  PubMed  PubMed Central  Google Scholar 

  19. Shirani F, Salehi-Abargouei A, Azadbakht L. Effects of Dietary approaches to stop hypertension (DASH) diet on some risk for developing type 2 diabetes: a systematic review and meta-analysis on controlled clinical trials. Nutrition. 2013;29(7–8):939–47.

    Article  PubMed  Google Scholar 

  20. Bricarello LP, Poltronieri F, Fernandes R, Retondario A, de Moraes Trindade EBS, de Vasconcelos FAG. Effects of the Dietary Approach to stop hypertension (DASH) diet on blood pressure, overweight and obesity in adolescents: a systematic review. Clin Nutr ESPEN. 2018;28:1–11.

    Article  Google Scholar 

  21. Sahebkar A, Heidari Z, Kiani Z, Atefi M, Zareie A, Shojaei M et al. The efficacy of Dietary approaches to Stop Hypertension (DASH) Diet on lipid Profile: a systematic review and metaanalysis of clinical controlled trials. Curr Med Chem. 2024.

  22. Mokhtari Z, Sharafkhah M, Poustchi H, Sepanlou SG, Khoshnia M, Gharavi A, et al. Adherence to the Dietary approaches to stop hypertension (DASH) diet and risk of total and cause-specific mortality: results from the Golestan Cohort Study. Int J Epidemiol. 2019;48(6):1824–38.

    Article  PubMed  PubMed Central  Google Scholar 

  23. Eghtesad S, Hekmatdoost A, Faramarzi E, Homayounfar R, Sharafkhah M, Hakimi H, et al. Validity and reproducibility of a food frequency questionnaire assessing food group intake in the PERSIAN Cohort Study. Front Nutr. 2023;10:1059870.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Fung TT, Chiuve SE, McCullough ML, Rexrode KM, Logroscino G, Hu FB. Adherence to a DASH-style diet and risk of coronary heart disease and stroke in women. Arch Intern Med. 2008;168(7):713–20.

    Article  PubMed  Google Scholar 

  25. Mahyoub MA, Elhoumed M, Maqul AH, Almezgagi M, Abbas M, Jiao Y, et al. Fatty infiltration of the pancreas: a systematic concept analysis. Front Med. 2023;10:1227188.

    Article  Google Scholar 

  26. Sreedhar UL, DeSouza SV, Park B, Petrov MS. A systematic review of intra-pancreatic Fat Deposition and pancreatic carcinogenesis. J Gastrointest Surgery: Official J Soc Surg Aliment Tract. 2020;24(11):2560–9.

    Article  Google Scholar 

  27. Mathur A, Marine M, Lu D, Swartz-Basile DA, Saxena R, Zyromski NJ, et al. Nonalcoholic fatty pancreas disease. HPB: Official J Int Hepato Pancreato Biliary Association. 2007;9(4):312–8.

    Article  Google Scholar 

  28. Gotoh K, Inoue M, Shiraishi K, Masaki T, Chiba S, Mitsutomi K, et al. Spleen-derived interleukin-10 downregulates the severity of high-fat diet-induced non-alcoholic fatty pancreas disease. PLoS ONE. 2012;7(12):e53154.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  29. Soeda J, Mouralidarane A, Cordero P, Li J, Nguyen V, Carter R, et al. Maternal obesity alters endoplasmic reticulum homeostasis in offspring pancreas. J Physiol Biochem. 2016;72(2):281–91.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  30. Carter R, Mouralidarane A, Soeda J, Ray S, Pombo J, Saraswati R, et al. Non-alcoholic fatty pancreas disease pathogenesis: a role for developmental programming and altered circadian rhythms. PLoS ONE. 2014;9(3):e89505.

    Article  PubMed  PubMed Central  Google Scholar 

  31. Lari A, Sohouli MH, Fatahi S, Cerqueira HS, Santos HO, Pourrajab B, et al. The effects of the Dietary approaches to stop hypertension (DASH) diet on metabolic risk factors in patients with chronic disease: a systematic review and meta-analysis of randomized controlled trials. Nutrition, metabolism, and cardiovascular diseases. NMCD. 2021;31(10):2766–78.

    CAS  PubMed  Google Scholar 

  32. Soltani S, Shirani F, Chitsazi MJ, Salehi-Abargouei A. The effect of dietary approaches to stop hypertension (DASH) diet on weight and body composition in adults: a systematic review and meta-analysis of randomized controlled clinical trials. Obes Reviews: Official J Int Association Study Obes. 2016;17(5):442–54.

    Article  Google Scholar 

  33. Perry CA, Van Guilder GP, Kauffman A, Hossain MA, Calorie-Restricted DASH. Diet reduces Body Fat and maintains muscle strength in obese older adults. Nutrients. 2019;12(1).

  34. Rodriguez-Lopez CP, Gonzalez-Torres MC, Aguilar-Salinas CA, Najera-Medina O. DASH Diet as a proposal for improvement in Cellular Immunity and its Association with metabolic parameters in persons with overweight and obesity. Nutrients. 2021;13(10).

  35. Campbell AP. DASH eating plan: an eating pattern for Diabetes Management. Diabetes Spectrum: Publication Am Diabetes Association. 2017;30(2):76–81.

    Article  Google Scholar 

  36. Ickin Gulen M, Guven Bagla A, Yavuz O, Hismiogullari AA. Histopathological changes in rat pancreas and skeletal muscle associated with high fat diet induced insulin resistance. Biotech Histochemistry: Official Publication Biol Stain Comm. 2015;90(7):495–505.

    Article  CAS  Google Scholar 

  37. Eitel K, Staiger H, Rieger J, Mischak H, Brandhorst H, Brendel MD, et al. Protein kinase C δ activation and translocation to the Nucleus are required for fatty acid-Induced apoptosis of insulin-secreting cells. Diabetes. 2003;52(4):991–7.

    Article  CAS  PubMed  Google Scholar 

  38. Gaborit B, Abdesselam I, Kober F, Jacquier A, Ronsin O, Emungania O et al. Ectopic fat storage in the pancreas using 1H-MRS: importance of diabetic status and modulation with bariatric surgery-induced weight loss. International journal of obesity (2005). 2015;39(3):480-7.

  39. Tremmel DM, Feeney AK, Mitchell SA, Chlebeck PJ, Raglin SA, Fernandez LA, et al. Hypertension, but not body mass index, is predictive of increased pancreatic lipid content and islet dysfunction. Am J Transplantation: Official J Am Soc Transplantation Am Soc Transpl Surg. 2020;20(4):1105–15.

    Article  CAS  Google Scholar 

  40. Levy BI, Schiffrin EL, Mourad JJ, Agostini D, Vicaut E, Safar ME, et al. Impaired tissue perfusion: a pathology common to hypertension, obesity, and diabetes mellitus. Circulation. 2008;118(9):968–76.

    Article  PubMed  Google Scholar 

  41. Liu Y, Ma Z, Zhao C, Wang Y, Wu G, Xiao J, et al. HIF-1α and HIF-2α are critically involved in hypoxia-induced lipid accumulation in hepatocytes through reducing PGC-1α-mediated fatty acid β-oxidation. Toxicol Lett. 2014;226(2):117–23.

    Article  CAS  PubMed  Google Scholar 

  42. Mylonis I, Simos G, Paraskeva E. Hypoxia-inducible factors and the regulation of lipid metabolism. Cells. 2019;8(3).

  43. Joye PNPV. IJ. Dietary Fibre from whole grains and their benefits on Metabolic Health. Nutrients. 2020;12(10).

  44. Barber TM, Kabisch S, Pfeiffer AFH, Weickert MO. The Health benefits of Dietary Fibre. Nutrients. 2020;12(10).

  45. Thompson SV, Hannon BA, An R, Holscher HD. Effects of isolated soluble fiber supplementation on body weight, glycemia, and insulinemia in adults with overweight and obesity: a systematic review and meta-analysis of randomized controlled trials1. Am J Clin Nutr. 2017;106(6):1514–28.

    Article  CAS  PubMed  Google Scholar 

  46. Hosseini B, Berthon BS, Saedisomeolia A, Starkey MR, Collison A, Wark PAB, et al. Effects of fruit and vegetable consumption on inflammatory biomarkers and immune cell populations: a systematic literature review and meta-analysis. Am J Clin Nutr. 2018;108(1):136–55.

    Article  PubMed  Google Scholar 

  47. DiNicolantonio JJ, Mehta V, Onkaramurthy N, O’Keefe JH. Fructose-induced inflammation and increased cortisol: a new mechanism for how sugar induces visceral adiposity. Prog Cardiovasc Dis. 2018;61(1):3–9.

    Article  PubMed  Google Scholar 

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Acknowledgements

We would like to express our deepest gratitude to all those who participated in this study. Their contribution and commitment to the research were truly invaluable.

Funding

This study is funded by Shahid Beheshti University of Medical Sciences, which has no role in the study design; collection, management and analysis of data; interpretation of results; writing of reports or decision to submit the report for publication.

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Authors and Affiliations

Authors

Contributions

Conceptualization, ZY and AH; Formal analysis, ZY; Methodology, MC, MB, AR and AS; Project administration, DF and MST; Writing – original draft, ZY, DF and MST; Writing – review & editing, ZY and AH. All authors read and approved.

Corresponding authors

Correspondence to Zahra Yari or Azita Hekmatdoost.

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Ethics approval

The Research Ethics Committees of Vice-Chancellor in Research Affairs of Shahid Beheshti University of Medical Sciences reviewed and approved the study methods and design (Ethics code: IR.SBMU.RETECH.REC.1402.689).

Competing interests

The authors declare no competing interests.

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Fotros, D., Tabar, M.S., Chegini, M. et al. Adherence to the dietary approaches to stop hypertension (DASH) and risk of pancreatic steatosis. J Health Popul Nutr 43, 190 (2024). https://doi.org/10.1186/s41043-024-00628-x

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