Effects of stepwise lipid-controlled enteral nutrition on lipids and nutrition in hyperlipidemic acute pancreatitis with colorectal cancer

Abstract

BACKGROUND

Hyperlipidemic acute pancreatitis (HLAP) combined with colorectal cancer presents a dual burden of metabolic inflammation and tumor consumption. Serum triglycerides (TGs) is the core trigger of HLAP, while colorectal cancer exacerbates malnutrition and lipid disorders. Traditional enteral nutrition adopts fixed lipid ratios, failing to balance TG control with adequate nutritional support. Based on dynamic TG monitoring and lipid metabolism principles, we hypothesize that a stepwise lipid-controlled enteral nutrition regimen, adjusting fat composition and energy ratio according to TG thresholds, will effectively reduce TG, improve lipid profiles, and optimize nutritional status in these complex patients.

AIM

To determine the effects of stepwise lipid-controlled enteral nutrition on lipids and nutrition in HLAP with colorectal cancer.

METHODS

We investigated one hundred patients with HLAP and colon cancer (January 2022 to December 2025) divided into two groups. Controls received routine enteral nutrition. The observation group received stepwise lipid-controlled enteral nutrition, with fat ratio and formula adjusted by TG levels. Outcomes included TG, lipid panel [total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C)], nutritional markers [albumin (ALB), prealbumin (PA), transferrin (TRF), arm muscle circumference (AMC)], symptom relief time, and complications, measured before and on days 3 and 7 of intervention.

RESULTS

After intervention, the observation group had lower TG levels than controls (day 3: 7.29 ± 2.37 mmol/L vs 12.61 ± 2.58 mmol/L; day 7: 4.75 ± 1.14 mmol/L vs 7.58 ± 2.16 mmol/L), better lipid profiles [day 3: HDL-C (0.87 ± 0.25 mmol/L vs 0.64 ± 0.22 mmol/L), LDL-C (2.38 ± 0.35 mmol/L vs 2.17 ± 0.47 mmol/L); day 7: TC (4.19 ± 0.54 mmol/L vs 3.86 ± 0.56 mmol/L), HDL-C (1.28 ± 0.37 mmol/L vs 0.96 ± 0.32 mmol/L), LDL-C (3.27 ± 0.42 mmol/L vs 2.84 ± 0.49 mmol/L)], and superior nutritional improvements [day 3: ALB (33.86 ± 3.06 g/L vs 32.26 ± 2.93 g/L) , PA (214.37 ± 27.93 mg/L vs 192.53 ± 24.06 mg/L) , TRF (1.76 ± 0.24 g/L vs 1.70 ± 0.25 g/L); day 7: ALB (38.26 ± 2.83 g/L vs 35.28 ± 2.68 g/L), PA (251.74 ± 31.65 mg/L vs 228.15 ± 27.43 mg/L), TRF (2.14 ± 0.28 g/L vs 1.86 ± 0.26 g/L), AMC (22.29 ± 2.36 cm vs 21.14 ± 2.30 cm)]. Clinical symptoms resolved faster, and complication rates were lower (12% vs 36%, P = 0.005).

CONCLUSION

Individualized stepwise lipid-controlled enteral nutrition effectively lowers TG, enhances lipid metabolism and nutrition, relieves symptoms, and reduces complications in HLAP-colorectal cancer patients.

Key Words: Hyperlipidemic pancreatitis; Colon cancer; Stepwise lipid control; Personalized nutrition; Enteral nutrition; Triglycerides

Core Tip: This intervention study demonstrates that a stepwise lipid-controlled enteral nutrition protocol, dynamically adjusted based on triglyceride (TG) thresholds, significantly reduces hypertriglyceridemia, optimizes concurrent lipid and protein metabolism, and accelerates clinical recovery in patients with hyperlipidemic acute pancreatitis and colorectal cancer. The findings advocate for integrating dynamic lipid monitoring into nutritional management for such complex comorbidities and propose a “TG-guided, protein-prioritized” enteral nutrition model, addressing a critical gap in the metabolic support of oncological patients with acute metabolic inflammation.

INTRODUCTION

Hyperlipidemic acute pancreatitis (HLAP) is an important subtype of acute pancreatitis, accounting for about 10%-20% of the causes of acute pancreatitis. Its onset is closely related to a significant increase in serum triglycerides (TGs)[1]. HLAP patients are prone to malnutrition and metabolic imbalance due to factors such as lipid metabolism disorders, nutritional consumption and inflammatory stress, which seriously affect the prognosis and recovery of the disease[2]. Meanwhile, as a common malignant tumor of the digestive tract, colon tumors can also lead to deterioration of patients' nutritional status and lipid metabolism disorders[3]. When HLAP and colon tumors occur simultaneously, they interact with each other in terms of metabolism, nutrition, and inflammatory response. On the one hand, HLAP requires strict restriction of exogenous lipids to avoid the rapid increase of TG and the aggravation or recurrence of pancreatitis. On the other hand, tumor depletion, surgical stress, and inflammatory response caused by colon tumors require sufficient nutritional supply to maintain immune function and promote tissue repair, which exacerbates the complexity of the patient’s condition and treatment difficulty, becoming a difficult point in clinical nutritional support. At present, nutritional support for patients with HLAP and colon cancer still mostly follows the traditional enteral nutrition program, which only focuses on total energy and protein supply and lacks systematic regulation and individualized management of lipid metabolism[4,5]. However, the core pathophysiological mechanism of HLAP is hypertriglyceridemia, and inappropriate lipid intake may induce or aggravate pancreatic inflammatory response[6]. Therefore, effectively controlling TG levels and improving lipid metabolism disorders while ensuring nutritional support has become a key issue in the nutritional management of such patients. Stepwise lipid control programs can dynamically adjust the type and energy ratio of lipids in enteral nutrition based on TG levels according to the patient’s actual condition, and have shown good potential in some metabolic diseases[7,8]. However, there are few studies on their application in patients with HLAP and colorectal cancer. Due to the fact that colon cancer patients often have abnormal lipoprotein activity, insulin resistance, and chronic low-grade inflammation, their metabolic response to lipid regulation may differ from that of patients with simple HLAP, and there is uncertainty risk in directly applying existing regimens. Therefore, it is necessary to verify the effectiveness and safety of stepwise lipid control in such complex patients.

Therefore, this study aims to explore the effects of individualized enteral nutrition support programs based on stepwise lipid control on serum TG levels, lipid metabolism indicators, and nutritional status in patients with HLAP and colorectal cancer, in order to provide more targeted and scientific intervention evidence for the clinical nutritional management of such complex patients.

MATERIALS AND METHODS

General information

One hundred patients with hypertriglyceridemia, acute pancreatitis, and colon cancer admitted to Yichang Central People’s Hospital from January 2022 to December 2025 were selected as the study subjects. They were divided into an observation group and a control group according to different intervention measures, with 50 patients in each group.

Exclusion and inclusion criteria

Inclusion criteria: (1) Meeting the diagnostic criteria for HLAP[9]; (2) Meeting the diagnostic criteria for colon cancer[10]; (3) A score of ≥ 3 on the Nutritional Risk Screening 2002[11]; (4) Not having distant metastases; (5) Being ≥ 18 years old; and (6) Having no cognitive or communication impairments.

Exclusion criteria: (1) Serious dysfunction of vital organs such as heart, lung, liver, and kidney; (2) Contraindications to enteral nutrition (such as complete intestinal obstruction, gastrointestinal bleeding, etc.); (3) History of gastrointestinal surgery affecting nutrient absorption; (4) Other malignant tumors; and (5) Immune system diseases and coagulation system diseases.

Methods

Control group: The control group received routine enteral nutrition after surgery. The daily energy requirement was estimated based on the patient's body weight, and the total daily energy was set at 25-30 kcal/kg and the nitrogen content at 0.15-0.20 g/kg, in accordance with the guidelines[12]. Enteral nutrition solution (Bipler, National Drug Approval Number H20010285, Nutricia Pharmaceutical Co., Ltd., 500 mL/bottle) was used.

Observation group: The observation group adopted an individualized enteral nutrition support program based on stepwise lipid control. (1) Establishment of a nutrition support team: The nutrition management team consisted of clinicians, clinical nutritionists, and specialist nurses. Within 24 hours of enrollment, the patients underwent nutritional and metabolic assessments and individualized goals were set, as follows: First, nutritional risk was assessed using Nutritional Risk Screening 2002; fasting TG, total cholesterol (TC), prealbumin (PA), etc., were measured to establish a baseline for lipid metabolism and nutrition. Second, similar to the control group, the observation group patients also had their daily total energy set at 25-30 kcal/kg and nitrogen at 0.15-0.20 g/kg. Based on baseline TG levels, three initial lipid control targets were established: If TG ≥ 5.65 mmol/L and fat energy ratio < 15%, medium-chain TG (MCT) formula was preferred; if TG 2.26-5.64 mmol/L and fat energy ratio 15%-20%, a mixed MCT/long-chain TG (LCT) formula was used; if TG < 2.26 mmol/L and fat energy ratio 20%-25%, a standard whole protein formula was used; (2) Implementation of stepwise enteral nutrition support: Enteral nutrition was initiated via nasoenteric tube, using individualized formulas corresponding to the steps, and the nutritional formula was continuously pumped in at a rate of 20-25 mL/hour; and (3) Dynamic monitoring and stepwise adjustment: Serum TG was monitored every 48-72 hours; nutritional indicators such as PA were monitored twice a week. If TG levels rise to the next higher threshold, immediately adjust the nutritional regimen to the corresponding stricter step. If the TG level remains stable below the lower limit of the current step threshold for more than 5 days and meets any of the following criteria for defining malnutrition: (a) Compared to the previous assessment, indicators such as PA, transferrin (TRF), arm muscle circumference (AMC) have no significant upward trend; and (b) Core nutritional indicators continue to be lower than clinical target values [such as albumin (ALB) < 35 g/L, PA < 200mg/L]. After excluding other influencing factors such as active infections, moderate increases in fat and LCT ratios can be evaluated. If signs of HLAP recurrence appear (e.g., worsening abdominal pain accompanied by TG > 11.3 mmol/L), enteral nutrition should be suspended until stabilization, at which point an individualized enteral nutrition support regimen based on step-wise lipid control should be restarted. Simultaneously, for diarrhea that may occur with coexisting colon cancer, a formula containing soluble dietary fiber can be selected and infusion parameters adjusted. Ensure daily protein intake reaches 1.2-1.5 g/kg. This regimen should be continued until the patient’s oral diet meets ≥ 60% of nutritional needs and TG remains stable below 2.26 mmol/L for more than 7 days, or until discharge. All interventions are performed by uniformly trained team members and recorded in a dedicated case report form.

Observation indicators

Serum TG levels: Venous blood was drawn from patients before nutritional support, on day 3 after nutritional support, and on day 7 after nutritional support. The blood was centrifuged at 3000 rpm for 5 minutes. The supernatant serum was aspirated using a pipette and transferred to 1.5 mL centrifuge tubes. The tubes were immediately frozen at -30 °C and tested according to the kit instructions.

Lipid metabolism indicators: These include TC and high/low density lipoprotein cholesterol [high-density lipoprotein (HDL) cholesterol (HDL-C) and low-density lipoprotein (LDL) cholesterol (LDL-C)]. The detection methods are the same as for TG.

Nutritional status indicators: Upper AMC, ALB, PA, and TRF were measured before nutritional support, on day 3 after nutritional support, and on day 7 after nutritional support. AMC was calculated by measuring the mid-arm circumference (MAC) and triceps skinfold thickness (TSF; AMC = MAC - 3.14 × TSF), primarily reflecting skeletal muscle reserves. Evaluation should be compared with age- and sex-matched standard values to assess the degree of muscle depletion. Normal AMC is ≥ 90% of the age- and sex-matched standard values. ALB, PA, and TRF levels were measured using a fully automated biochemical analyzer manufactured by Beckman Coulter.

Improvement of clinical symptoms: The time to relief of abdominal pain, time to relief of abdominal distension, and length of hospital stay were recorded for both groups of patients.

Occurrence of complications: Count the incidence of malnutrition, diarrhea, infection, and intestinal fistula in two groups of patients.

Statistical analysis

Data were processed using SPSS 21.0 statistical software. Count data were expressed as n (%) and analyzed using the χ² test; continuous data were expressed as mean ± SD and analyzed using the t test. Repeated measures data at different time points were analyzed using repeated measures ANOVA and simple effects analysis. The significance level was set at α = 0.05, and P < 0.05 was considered statistically significant.

RESULTS

Comparison of general data between the two groups

This study included 100 patients, with 50 patients in each group. The control group had 64.0% males, while the observation group had 56.0% males; The average age of the control group was 58.20 ± 10.45 years, while the observation group was 57.62 ± 11.34 years; The BMI was 26.80 ± 3.49 kg/m² and 27.10 ± 3.20 kg/m², respectively. Severity of illness (mild/moderate severe/severe): Control group 20.0%/56.0%/24.0%, observation group 22.0%/52.0%/26.0%. Pathological malignancy ratio: Control group 70.0%, observation group 66.0%. The proportion of diabetes was 36.0% in the control group and 40.0% in the observation group. There was no statistically significant difference in the above indicators between the two groups (P > 0.05), as shown in Table 1.

Table 1 Comparison of general data between the two groups, n (%) or mean ± SD.

Project	Category	Control group (n = 50)	Observation group (n = 50)	t/χ2 value	P value
Age (year)		58.20 ± 10.45	57.62 ± 11.34	0.266	0.791
Gender	Male	32 (64.00)	28 (56.00)	0.667	0.414
	Female	18 (36.00)	22 (44.00)
BMI (kg/m2)		26.80 ± 3.49	27.10 ± 3.20	-0.445	0.657
Severity of the condition	Mild cases	10 (20.00)	11 (22.00)	-0.162	0.922
	Moderate to severe	28 (56.00)	26 (52.00)
	Severe	12 (24.00)	13 (26.00)
Pathological nature	Benign	15 (30.00)	17 (34.00)	0.184	0.668
	Malignant	35 (70.00)	33 (66.00)
Diabetes	No	32 (64.00)	30 (60.00)	0.170	0.680
	Yes	18 (36.00)	20 (40.00)

BMI: Boda mass index.

Comparison of serum TG levels between the two groups

Before the intervention, there was no statistically significant difference in TG levels between the two groups (P > 0.05). On day 3 after the intervention, the TG level in the observation group (7.29 ± 2.37 mmol/L) was significantly lower than that in the control group (12.61 ± 2.58 mmol/L, P < 0.05). On day 7 after the intervention, the TG levels in both groups further decreased, but the observation group (4.75 ± 1.14 mmol/L) remained significantly lower than the control group (7.58 ± 2.16 mmol/L, P < 0.05; Table 2).

Table 2 Comparison of triglyceride levels before and after intervention in the two groups (n = 50), mean ± SD.

Group	Before nutritional support (mmol/L)	Day 3 after nutritional support (mmol/L)	Day 7 after nutritional support (mmol/L)
Control group	17.24 ± 3.09	12.61 ± 2.58a	7.58 ± 2.16a,b
Observation group	17.59 ± 3.57	7.29 ± 2.37a	4.75 ± 1.14a,b
F value	0.278	115.284	66.797
P value	0.599	< 0.001	< 0.001

^aP < 0.05 vs before nutritional support.

^bP < 0.05 vs day 3 after nutritional support.

Comparison of lipid metabolism indicators between the two groups

Before nutritional support, there were no statistically significant differences in TC, HDL-C, and LDL-C levels between the two groups (P > 0.05). After nutritional support, regarding TC, the observation group (4.19 ± 0.54 mmol/L) showed a significantly higher level than the control group (3.86 ± 0.56 mmol/L, P < 0.05) on day 7; regarding HDL-C and LDL-C, the observation group showed significantly higher levels than the control group on both days 3 (HDL-C: 0.87 ± 0.25 mmol/L vs 0.64 ± 0.22 mmol/L; LDL-C: 2.38 ± 0.35 mmol/L vs 2.17 ± 0.47 mmol/L) and 7 (HDL-C: 1.28 ± 0.37 mmol/L vs 0.96 ± 0.32 mmol/L; LDL-C: 3.27 ± 0.42 mmol/L vs 2.84 ± 0.49 mmol/L) after nutritional support (P < 0.05; Table 3).

Table 3 Comparison of total cholesterol, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol levels before and after intervention in the two groups (n = 50), mean ± SD.

Group		TC (mmol/L)	HDL-C (mmol/L)	LDL-C (mmol/L)
Control group	Before nutritional support	3.38 ± 0.59	0.72 ± 0.19	2.41 ± 0.54
	Day 3 after nutritional support	3.44 ± 0.51	0.64 ± 0.22	2.17 ± 0.47a
	Day 7 after nutritional support	3.86 ± 0.56a,b	0.96 ± 0.32a,b	2.84 ± 0.49a,b
Observation group	Before nutritional support	3.27 ± 0.50	0.75 ± 0.23	2.56 ± 0.42
	Day 3 after nutritional support	3.54 ± 0.46a	0.87 ± 0.25a,c	2.38 ± 0.35a,c
	Day 7 after nutritional support	4.19 ± 0.54a,b,c	1.28 ± 0.37a,b,c	3.27 ± 0.42a,b,c

^aP < 0.05 vs before nutritional support.

^bP < 0.05 vs day 3 after nutritional support.

^cP < 0.05 vs the control group at the same time point.

TC: Total cholesterol; HDL-C: High-density lipoprotein cholesterol; LDL-C: Low-density lipoprotein cholesterol.

Comparison of nutritional status indicators between the two groups

Before nutritional support, there were no statistically significant differences in AMC, ALB, PA, and TRF levels between the two groups (P > 0.05). After intervention, all indicators showed an improving trend in both groups, but the improvement was more significant in the observation group. On day 3 of nutritional support, the ALB (33.86 ± 3.06 g/L vs 32.26 ± 2.93 g/L), PA (214.37 ± 27.93 mg/L vs 192.53 ± 24.06 mg/L), and TRF levels (1.76 ± 0.24 g/L vs 1.70 ± 0.25 g/L) in the observation group were significantly better than those in the control group at the same time point (P < 0.05). By day 7 of nutritional support, the observation group was significantly better than the control group in all four indicators (ALB: 38.26 ± 2.83 g/L vs 35.28 ± 2.68 g/L; PA: 251.74 ± 31.65 mg/L vs 228.15 ± 27.43 mg/L; TRF: 2.14 ± 0.28 g/L vs 1.86 ± 0.26 g/L; AMC: 22.29 ± 2.36 cm vs 21.14 ± 2.30 cm, P < 0.05; Table 4).

Table 4 Comparison of arm muscle circumference, albumin, prealbumin and transferrin levels before and after intervention in the two groups (n = 50), mean ± SD.

Group		ALB (g/L)	PA (mg/L)	TRF (g/L)	AMC (cm)
Control group	Before nutritional support	31.52 ± 3.27	180.46 ± 23.66	1.68 ± 0.31	20.84 ± 2.52
	Day 3 after nutritional support	32.26 ± 2.93	192.53 ± 24.06a	1.70 ± 0.25a	20.68 ± 2.75
	Day 7 after nutritional support	35.28 ± 2.68a,b	228.15 ± 27.43a,b	1.86 ± 0.26a,b	21.14 ± 2.30
Observation group	Before nutritional support	30.85 ± 3.54	181.52 ± 26.77	1.65 ± 0.28	21.21 ± 1.98
	Day 3 after nutritional support	33.86 ± 3.06a,c	214.37 ± 27.93a,c	1.76 ± 0.24a,c	21.61 ± 2.15
	Day 7 after nutritional support	38.26 ± 2.83a,b,c	251.74 ± 31.65a,b,c	2.14 ± 0.28a,b,c	22.29 ± 2.36c

^aP < 0.05 vs before nutritional support.

^bP < 0.05 vs day 3 after nutritional support.

^cP < 0.05 vs the control group at the same time point.

ALB: Albumin; PA: Prealbumin; TRF: Transferrin; AMC: Arm muscle circumference.

Comparison of clinical symptom improvement between the two groups

The observation group showed significantly better improvement in all clinical symptom indicators than the control group (abdominal pain relief time: 3.8 ± 0.9 days vs 5.3 ± 1.2 days; time to relief of abdominal bloating symptoms: 4.8 ± 1.3 days vs 6.6 ± 1.5 days; length of hospital stays: 12.4 ± 2.6 days vs 14.6 ± 3.7 days, P < 0.05; Table 5).

Table 5 Comparison of clinical symptom improvement before and after intervention in the two groups (n = 50), mean ± SD.

Group	Abdominal pain relief time (day)	Time to relief of abdominal bloating symptoms (day)	Length of hospital stay (day)
Control group	5.3 ± 1.2	6.6 ± 1.5	14.6 ± 3.7
Observation group	3.8 ± 0.9	4.8 ± 1.3	12.4 ± 2.6
t value	6.685	6.406	3.437
P value	< 0.001	< 0.001	0.001

Comparison of the incidence of complications between the two groups

The overall incidence of complications in the observation group was lower than that in the control group (12% vs 36%, χ² = 7.895, P < 0.05; Table 6).

Table 6 Comparison of complication rates between the two groups, n (%).

Group	Total	Malnutrition	Diarrhea	Infect	Enterocutaneous fistula	Total occurrence
Control group	50	6 (12.00)	4 (8.00)	6 (12.00)	2 (4.00)	18 (36.00)
Observation group	50	0	2 (4.00)	3 (6.00)	1 (2.00)	6 (12.00)
χ2 value						7.895
P value						0.005

DISCUSSION

Patients with HLAP complicated with colon tumors have a dual pathological state of metabolic inflammation and tumor consumption, which presents many challenges in clinical nutritional support for these patients. Hypertriglyceridemia is not only the core inducing factor of HLAP, but also an important aggravating factor of its disease progression. Therefore, it is necessary to strictly control the intake of exogenous lipids in patients. In addition, patients with colon tumors often have protein-energy malnutrition, and the body’s immune maintenance and tissue repair processes require sufficient nutritional supply as support[13]. Although traditional enteral nutrition programs can achieve basic nutritional supplementation, their lipid ratios are fixed and cannot adapt to the dynamic metabolic needs of these patients, which can easily lead to problems such as poor TG regulation or insufficient nutritional supply[14]. This study applied a stepwise lipid control program, and adjusted the types of fat and the proportion of fat energy supply in the enteral nutrition formula in a timely manner according to the dynamic monitoring of TG levels of patients. It fully implemented the individualized and dynamic principles of nutritional management and preliminarily confirmed the feasibility and clinical effectiveness of this program in complex patient groups with metabolic abnormalities and tumors.

The results of this study showed that the TG levels in the observation group were significantly lower than those in the control group on days 3 and 7 of the intervention (P < 0.05), and lipid metabolism indicators such as TC, HDL-C, and LDL-C also showed a better improvement trend in the observation group. This indicates that the fat intake adjustment program based on TG levels can effectively reduce the TG load in the blood circulation and alleviate the continuous damage of lipid overload to the pancreas. Furthermore, while TG decreased in the observation group, HDL-C and LDL-C did not decrease simultaneously; instead, they showed a moderate increase in the later stages of the intervention, suggesting that stepwise lipid control may help maintain or improve lipoprotein metabolic balance while reducing TG. This may be related to the rational selection of medium-chain fatty acids (MCFAs) and the gradual adjustment of the proportion of long-chain fatty acids (LCFAs) in the formulation. First, MCFAs have the structural advantages of high water solubility and small molecular weight compared with LCFAs because their carbon chains contain only 8-12 carbon atoms. This allows them to pass directly through the intestinal mucosal epithelial cells into the portal vein system without being transported through the lymphatic system. They are then rapidly taken up by the liver and oxidized for energy, thus avoiding abnormal accumulation of lipids in the intestine and liver[15]. At the same time, the rapid oxidative metabolism of MCFAs can reduce the synthesis and storage of fatty acids in the liver, thereby inhibiting the synthesis and secretion of very low-density lipoprotein (VLDL) in the liver. VLDL is the main carrier of TG in the blood circulation. Its reduced secretion can directly reduce the TG content in the blood. This is one of the key mechanisms by which the stepwise lipid control program can rapidly and effectively reduce TG levels[16]. In addition, MCFAs have high oxidative energy efficiency and can provide sufficient energy to the body in a short period of time, reducing the body’s decomposition and utilization of protein, indirectly helping to maintain the body’s positive nitrogen balance, and forming a synergistic effect with the principle of sufficient protein supply in the program, further protecting pancreatic function[17]. Secondly, LCFAs, as the main source of essential fatty acids such as linoleic acid and α -linolenic acid, cannot be synthesized by the body itself and must be supplemented through dietary intake. These essential fatty acids are not only important components of cell membrane phospholipids, but also key substances for maintaining cell membrane fluidity, integrity and signal transduction function[18]. At the same time, essential fatty acids can also participate in the synthesis of bioactive substances such as prostaglandins and leukotrienes, which are of great significance for regulating the body’s inflammatory response and maintaining intestinal mucosal function[19]. Moreover, gradually increasing the supply of LCFAs can provide sufficient substrates for lipoprotein assembly and metabolism, promote the normal synthesis and metabolism of lipoproteins such as HDL and LDL, avoid insufficient lipoprotein synthesis due to simply restricting fat intake, and thus maintain lipoprotein metabolic balance. In addition, reasonable intake of LCFAs helps maintain the synthesis of structural lipids such as phosphatidylcholine in the body. The latter is an important component of HDL and LDL particles, and sufficient synthesis of LCFAs can ensure the structural integrity and functional stability of HDL and LDL particles[20]. HDL can transport excess cholesterol from peripheral tissues to the liver for metabolism and clearance through reverse cholesterol transport, thereby preventing cholesterol from depositing in the blood vessel walls and pancreatic tissues and reducing lipid toxicity damage[21]. LDL can transport cholesterol to various tissue cells in the body, providing raw materials for cell metabolism and repair[22]. The two work together to maintain the body's lipid metabolism homeostasis.

In terms of nutritional status, the observation group showed better improvement in serum ALB, PA, TRF and AMC than the control group (P < 0.05), indicating that the stepwise lipid control did not affect the overall nutritional status of the patients, but instead optimized protein synthesis and muscle reserves through precise regulation. This is closely related to the emphasis on adequate protein supply (1.2-1.5 g/kg per day) and dynamic monitoring and adjustment in the protocol. On the one hand, the protocol ensures adequate supply of high-quality protein, providing substrate support for the liver to synthesize acute phase protein and maintain positive nitrogen balance[23]; on the other hand, through dynamic monitoring and stepwise adjustment, it avoids inflammation activation and metabolic stress caused by excessive lipid load, thereby reducing protein breakdown and consumption. In addition, the observation group had significantly shorter time to relieve abdominal pain, time to relieve abdominal distension and length of hospital stay than the control group (P < 0.05), which suggests that individualized nutritional support not only improves biochemical indicators, but also has clear clinical translation benefits. The reason for this may be that, firstly, by controlling TG levels, pancreatic lipotoxicity and inflammatory response are reduced, thereby relieving abdominal pain. As the core organ of lipid metabolism, the pancreas has acinar cells that are abnormally sensitive to lipid load. When the TG level is too high, the excess lipids in the blood circulation will exceed the pancreatic metabolic threshold and accumulate in the acinar cells, thereby inducing lipotoxic damage[24]. Secondly, reasonable nutritional formula and infusion method help maintain the intestinal mucosal barrier function, promote the recovery of intestinal peristalsis, and reduce the occurrence of abdominal distension. The intestinal mucosal barrier is an important defense line for the body to resist the invasion of external pathogens and maintain the stability of the internal environment. In the disease state, the intestinal function of patients is easily suppressed. In addition, insufficient nutritional intake will lead to nutritional deficiency of intestinal mucosal epithelial cells, atrophy and thinning, increased mucosal permeability, intestinal flora imbalance, large proliferation of harmful bacteria and excessive gas production, and slowed intestinal peristalsis, which will lead to gas not being discharged in time, thus causing abdominal distension[25]. Thirdly, the improvement of overall nutritional status enhances the patient's immune function and provides a physiological basis for early recovery and shortening hospital stay. In the disease state, patients often lack the raw materials such as proteins and amino acids required for the synthesis of immune cells due to insufficient nutritional intake and metabolic disorders. This leads to a decrease in the number and activity of immune cells such as lymphocytes and macrophages, a reduction in the body's immune response, an inability to effectively resist the invasion of pathogens, and a slow resolution of inflammatory response and delayed tissue repair, ultimately resulting in a prolonged hospitalization period[26].

This study showed that the overall incidence of complications in the observation group was significantly lower than that in the control group (P < 0.05), especially in the control of malnutrition and infection. This indicates that individualized enteral nutrition support based on stepwise lipid control has good safety in clinical practice, can effectively reduce the risk of complications in patients, and provides important support for improving prognosis.

However, this study has limitations. First, it is a retrospective study, with data from single-center medical records, which may introduce selection and information biases. Furthermore, the sample size is relatively limited, and the generalizability of the results needs further validation. Second, the intervention period was short, failing to systematically track patients’ long-term nutritional status, lipid metabolism evolution, and tumor-related outcomes after discharge. Third, the step adjustment indicators mainly rely on TG levels; future studies could incorporate multi-dimensional data such as fatty acid profiles, inflammatory markers, and metabolomics to further improve the systematicity and individualization of the step criteria. Future research should focus on prospective, multicenter, large-sample randomized controlled trials with extended follow-up periods to comprehensively evaluate the impact of this nutritional pattern on tumor prognosis, quality of life, medical costs, and long-term metabolic health.

CONCLUSION

In conclusion, individualized enteral nutrition support based on stepwise lipid control can effectively reduce serum TG levels, improve lipid metabolism disorders, enhance nutritional status, accelerate the relief of clinical symptoms, and reduce the incidence of complications in patients with hyperlipidemic pancreatitis and colon cancer. It is a clinically feasible and comprehensive nutritional management strategy.