Definition

Clinical nutrition in type 2 diabetes (T2D) is a therapeutic component of comprehensive cardiometabolic risk management rather than an intervention directed exclusively toward glycemic control. Nutritional strategies can influence body weight and visceral adiposity, insulin resistance, postprandial glucose metabolism, atherogenic dyslipidemia, blood pressure, and metabolic dysfunction-associated steatotic liver disease (MASLD). Their clinical value therefore extends beyond glycated hemoglobin (HbA1c) reduction and includes the modification of several interconnected determinants of cardiovascular and hepatic risk [1–6,36].

1. Introduction

Type 2 diabetes is a complex cardiometabolic disorder in which hyperglycemia commonly coexists with visceral adiposity, insulin resistance, atherogenic dyslipidemia, hypertension, and liver-related metabolic dysfunction ^{[1][2][3][4][5][6]}[1–6,36]. These abnormalities frequently occur in the same individual and contribute to persistent cardiovascular and hepatic risk even when glycemic control appears satisfactory.

Within this context, nutrition should be considered an active therapeutic intervention rather than a generic lifestyle recommendation. Dietary interventions can modify energy balance, body composition, postprandial metabolism, lipid handling, blood pressure, and hepatic fat accumulation ^{[1][2][3][4][5][7][8][9]}[1–5,7–9,36]. Consequently, their clinical effectiveness should not be evaluated solely according to changes in HbA1c.

A nutritional strategy may provide clinically relevant benefit even when its effect on HbA1c is modest, provided that it improves body weight, visceral adiposity, lipid profile, blood pressure, or markers associated with MASLD and overall cardiometabolic risk ^{[9][10][11][12][13][14]}[1–5,9–14,36].

2. Nutrition Beyond Glycemic Control

The metabolic effects of nutrition in T2D involve several complementary pathways. Depending on the dietary strategy and the degree of adherence achieved, nutritional intervention may reduce excess energy intake, promote weight loss, improve insulin sensitivity, attenuate postprandial glucose excursions, reduce triglycerides, and improve liver-related metabolic parameters ^{[2][3][4][5][9][10][11][12][13][14]}[2–5,9–14,36].

Weight reduction is particularly relevant in individuals with overweight or obesity because visceral adiposity contributes to insulin resistance, systemic inflammation, hepatic fat accumulation, dyslipidemia, and worsening cardiometabolic risk. Even moderate weight loss may produce clinically meaningful benefits, whereas larger and sustained reductions can result in broader metabolic improvement and may support remission-oriented care in selected individuals ^{[3][11][12][15][16]}[3,11,12,15,16,36].

Nutrition may also contribute to reducing treatment burden. Structured and sustainable nutritional interventions can support metabolic improvement alongside glucose-lowering, lipid-lowering, antihypertensive, and weight-lowering therapies and may, in selected patients, facilitate therapeutic de-intensification or remission-oriented strategies ^[15][16][17][2,4,11,12,15–17,36].

For these reasons, clinical nutrition in T2D is best understood as a multisystem intervention targeting the metabolic abnormalities that contribute to cardiovascular risk, hepatic dysfunction, and long-term disease progression [36].

3. Main Nutritional Strategies

3.1. Mediterranean-Style Dietary Patterns

Mediterranean-style dietary patterns represent one of the most clinically supported and transferable nutritional approaches for people with T2D. They are associated with favorable effects on dietary quality, glycemic control, triglycerides, blood pressure, and overall cardiovascular risk ^{[2][7][8][9][10][18][19]}[2,7–10,18,19,36].

The Mediterranean diet should not be interpreted as a mandatory or universal prescription. Rather, it can serve as a pragmatic reference model based on a high-quality dietary pattern that incorporates foods such as vegetables, legumes, minimally processed whole grains, plant-based protein sources, nuts, and unsaturated fats ^[18][19][20][2,7–10,18–20,36].

Its potential clinical advantage derives from the ability to address several components of cardiometabolic risk simultaneously rather than targeting glucose metabolism alone. Mediterranean-style patterns may also be particularly appropriate when MASLD, dyslipidemia, or elevated cardiovascular risk coexist with T2D [3–6,9,10,36].

3.2. Weight-Oriented Nutritional Strategies

Weight-oriented interventions are especially relevant in people with overweight, obesity, central adiposity, hepatic steatosis, or remission-oriented therapeutic goals.

The objective is not simply caloric restriction, but the achievement and maintenance of clinically meaningful weight loss capable of reducing visceral adiposity and improving insulin resistance, liver fat, blood pressure, and atherogenic dyslipidemia ^{[3][11][12][14][15][16]}[3,11,12,14–16,36].

Substantial and sustained weight reduction may modify the clinical course of T2D in selected individuals and can support diabetes remission ^{[11][12][15][17]}[11,12,15,17,36].

However, weight-loss interventions require specific caution in older or frail individuals. Excessive loss of lean mass should be avoided through adequate nutritional quality, appropriate protein intake, and attention to physical function. Protein requirements should also be individualized according to renal function, particularly in individuals with advanced chronic kidney disease [1,35,36].

3.3. Lower-Carbohydrate Approaches

Lower-carbohydrate dietary approaches may be useful in selected people with T2D, particularly when postprandial hyperglycemia, glycemic variability, or hypertriglyceridemia represent important therapeutic targets [2,13,21–27,36].

Their effectiveness should not be judged solely according to the percentage of carbohydrates consumed. Food quality, fiber intake, degree of food processing, fatty acid composition, sustainability, and clinical context remain important determinants of their long-term value ^{[2][13][18][19][20][21][22][23][24][25][26][27]}[2,13,22–27,36].

Available evidence does not establish low-carbohydrate approaches as universally superior to other high-quality dietary strategies over the long term [13,22–27]. They should therefore be considered one therapeutic option among several rather than a preferred dietary ideology [36].

3.4. Very-Low-Carbohydrate and Ketogenic Diets

Very-low-carbohydrate and ketogenic diets may produce rapid short-term improvements in glycemia, body weight, and triglycerides in selected individuals [22–27,36]. However, their routine long-term use requires greater caution because sustainability, dietary monotony, nutritional adequacy, and treatment compatibility may become problematic.

Particular attention is required in patients treated with sodium-glucose cotransporter 2 (SGLT2) inhibitors. Combining these drugs with very-low-carbohydrate or ketogenic diets may increase the risk of diabetic ketoacidosis, including euglycemic presentations ^[28][29][30][28–30,36].

These dietary approaches should therefore be used selectively and with appropriate clinical counseling and monitoring.

4. Dietary Quality and Meal Structure

The metabolic effects of nutrition cannot be reduced to macronutrient percentages alone. Carbohydrate quality, fiber intake, degree of food processing, fatty acid composition, meal structure, and eating behavior all contribute to the cardiometabolic impact of a dietary pattern [1,2,36].

Two diets with similar proportions of carbohydrates, fats, and proteins may therefore have substantially different metabolic effects depending on the foods from which these nutrients are derived.

Soluble fiber from foods such as legumes and oats may favorably influence postprandial glycemia and lipid profile [1,2,36]. Meal timing may also influence metabolic outcomes, although evidence specifically in people with T2D remains limited ^[31][31,36].

Overall, dietary quality and sustainability are more clinically relevant than adherence to rigid nutritional ideologies.

5. Effects on Major Cardiometabolic Domains

5.1. Body Weight and Visceral Adiposity

Excess adiposity, particularly visceral adiposity, is a major contributor to insulin resistance, systemic inflammation, hepatic fat accumulation, and worsening cardiometabolic risk in T2D [3,11,12,14–16,36].

Sustained nutritional interventions that reduce body weight may improve glycemic control, blood pressure, dyslipidemia, and liver-related metabolic abnormalities. The clinical objective should therefore be durable improvement rather than short-term weight reduction alone.

5.2. Atherogenic Dyslipidemia

Atherogenic dyslipidemia in T2D commonly includes elevated triglycerides, low high-density lipoprotein cholesterol, and increased atherogenic remnant burden.

Dietary composition and energy balance can influence this phenotype. Improved carbohydrate quality, reduction of rapidly absorbable carbohydrates, and replacement of saturated fats with unsaturated fats may favorably affect conventional lipid parameters and reduce the predominance of small, dense low-density lipoprotein particles [1,2,9,10,22–26,36].

Nutrition therefore represents an additional component of residual lipid-risk management alongside appropriate pharmacological therapy [36].

5.3. Insulin Resistance and Postprandial Metabolism

Nutritional strategies may improve insulin sensitivity and reduce postprandial glucose excursions and glycemic variability [1,2,10,13,22–26,36].

These effects may be clinically relevant even when changes in HbA1c are relatively modest, reinforcing the concept that HbA1c alone cannot capture the full metabolic impact of nutritional treatment [36].

5.4. Blood Pressure

Dietary quality, sodium intake, body weight, insulin resistance, and vascular health are closely interconnected in T2D. Nutritional interventions may contribute to blood-pressure reduction and broader cardiovascular risk management through several of these pathways [1,2,4,9,10,36].

5.5. Metabolic Dysfunction-Associated Steatotic Liver Disease

MASLD is particularly relevant in T2D because it lies at the intersection of visceral adiposity, hepatic insulin resistance, inflammation, dyslipidemia, and cardiovascular risk [5,6,32–34,36].

Nutritional management should therefore extend beyond generic recommendations for weight reduction. Clinically relevant targets include sustained energy deficit when weight loss is required, improvement in overall dietary quality, reduction in exposures that favor hepatic fat accumulation, and limitation of alcohol intake ^[32][33][34][3–6,14,32–34,36].

Important dietary exposures include excess caloric intake, ultra-processed foods, sugar-sweetened or fructose-rich products, and excessive saturated fat intake. Replacement of saturated fats with unsaturated fats may also be metabolically relevant [3–6,14,32–34,36].

Meaningful weight reduction remains a major determinant of improvement in hepatic steatosis, while substantial and sustained weight loss may also favor improvement in steatohepatitis and fibrosis-related risk [14,36].

6. Personalization and Clinical Implementation

There is no single nutritional prescription appropriate for every individual with T2D. Nutritional care should be individualized according to age, adiposity pattern, cardiovascular risk, hepatic involvement, renal function, frailty, pharmacological treatment, socioeconomic context, food habits, and the likelihood of long-term adherence [1–4,36].

For example, an individual with central obesity and hypertriglyceridemia may benefit from an approach emphasizing weight reduction and improved carbohydrate quality. Conversely, an older or frail patient may require a less restrictive strategy focused on nutritional adequacy, meal regularity, preservation of lean mass, and maintenance of functional status ^[1][35][36][1,35,36].

Practical nutritional interventions may include realistic changes such as reducing ultra-processed foods, improving carbohydrate quality, increasing intake of soluble fiber-rich foods, adjusting portion sizes, and pursuing gradual weight reduction [1,2,36].

Dietary treatment should also be integrated with physical activity, behavioral support, and pharmacological therapy rather than delivered as an isolated intervention [1–4,11,12,16,36].

Long-term adherence is a major determinant of clinical effectiveness. Affordability, cultural acceptability, family structure, cooking skills, work schedules, social environment, emotional eating, and the degree of dietary restriction can all influence sustainability [1,2,36].

Consequently, the most appropriate nutritional strategy is not necessarily the most restrictive or the one producing the fastest metabolic response, but the one capable of producing durable improvement across multiple cardiometabolic domains while remaining feasible for the individual [36].

7. Integration with Pharmacological Therapy

Nutritional therapy should not be viewed as competing with pharmacological treatment. Instead, it can complement the effects of glucose-lowering, weight-lowering, lipid-lowering, and antihypertensive medications ^[2][4][36][2,4,36].

At the same time, dietary strategies must remain compatible with the patient’s pharmacological regimen. This is particularly relevant when very-low-carbohydrate or ketogenic diets are considered in individuals receiving therapies that may influence ketosis risk or glycemic variability ^{[28][29][30][36]}[28–30,36].

Nutrition should therefore be integrated within the overall therapeutic strategy rather than prescribed as an isolated intervention.

8. Long-Term Adherence

Long-term adherence is one of the main determinants of the effectiveness of nutritional therapy. Even a physiologically attractive dietary strategy has limited clinical value if it cannot be maintained over time [1,2,36].

Adherence is influenced by affordability, cultural acceptability, family structure, cooking ability, work schedules, social context, and the degree of dietary restriction. Effective nutritional management therefore requires negotiation, repeated follow-up, and adjustment over time [1,2,36].

Behavioral support may also help patients manage emotional eating, hedonic hunger, and compensatory overeating, all of which may undermine long-term sustainability [1,36].

The most clinically useful nutritional strategy is consequently not necessarily the most restrictive or metabolically aggressive one, but the one capable of producing durable cardiometabolic improvement while remaining sustainable for the patient [36].

9. Limitations of Current Evidence

Nutritional studies in T2D show substantial heterogeneity in patient populations, metabolic characteristics, comparators, intervention duration, counseling intensity, and concomitant interventions [2,10,13,22–26,36].

Adherence is another important limitation because dietary intake maintained over time often differs from the originally assigned intervention. Differences between dietary groups may progressively decrease during follow-up [2,10,13,22–26].

Furthermore, improvements observed in nutritional trials may reflect not only dietary composition but also weight loss, behavioral support, increased healthcare contact, physical activity, medication adjustments, and therapeutic de-intensification [11,12,14–16,21–26,36].

Many studies also focus on short- or intermediate-term metabolic outcomes, whereas cardiovascular disease develops over considerably longer periods. Long-term cardiometabolic benefit is therefore frequently inferred from intermediate markers whose durability depends strongly on sustained adherence ^{[2][10][13][22][23][24][25][26][36]}[2,10,13,22–26,36].

Current evidence consequently supports individualized, high-quality, sustainable nutritional care rather than rigid hierarchies between dietary models [36].

10. Conclusions

Clinical nutrition is a core component of cardiometabolic risk management in T2D [36].

Its therapeutic value extends beyond glucose lowering and includes effects on body weight, visceral adiposity, insulin resistance, dyslipidemia, blood pressure, hepatic metabolic dysfunction, and overall treatment burden [1–6,36].

Mediterranean-style dietary patterns provide a particularly pragmatic reference approach [2,7–10,18,19,36]. Weight-oriented strategies are especially relevant in individuals with excess adiposity and remission-oriented goals, [3,11,12,15–17,36], while lower-carbohydrate approaches may be useful in selected patients [13,22–27,36]. Very-low-carbohydrate and ketogenic diets require greater caution because of issues related to sustainability, nutritional adequacy, and treatment-related safety [22–30,36].

The objective of nutritional therapy in T2D is therefore not to identify a universally superior diet, but to select a scientifically supported, individualized, and sustainable approach capable of improving several components of cardiometabolic risk simultaneously [36].

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