Hypoproteic Diet in Acromegaly
- Conditions
- Acromegaly
- Interventions
- Other: Usual clinical practice + hypoproteic diet
- Registration Number
- NCT05298891
- Lead Sponsor
- Azienda Ospedaliero Universitaria Maggiore della Carita
- Brief Summary
Since protein and AAs are master regulator of GH and IGF-I secretion, we hypothesized that a low protein diet could reduce GH and IGF-I levels in acromegalic patients in addition to conventional therapy. Furthermore, we aim to explore metabolomic, microbiota, and micro-vesicle fingerprints of GH hypersecretion during conventional therapy and after a low protein diet
- Detailed Description
Nutrients are crucial modifiers of the GH/IGF-I axis. In particular, a close cross-talk between proteins and amino acids (AAs) and GH/IGF-I secretion exists.
Both AAs and proteins affect GH secretion. AAs stimulate GH secretion upon oral administration, with different potency among studies, being the combination of arginine and lysine the most powerful. Soy proteins also stimulate GH secretion when ingested either as hydrolysed proteins or free AAs. Furthermore, the acute GH response to AAs ingestion may be influenced by the daily amount of dietary protein/AAs consumption: diets high in proteins apparently increase basal GH levels.
AAs and proteins have a positive effect on IGF-I secretion as well. In general, high levels of proteins, especially animal and dairy proteins, and consumption of branched chain amino acids (BCAAs) increase serum IGF-I levels.
Considering pathological GH conditions, metabolomic analysis of acromegalic patients suggests that the main metabolic fingerprint of GH hypersecretion is a reduction in BCAAs, related to the disease activity. Moreover, there is evidence that GH, rather than IGF-I, is the main mediator of such metabolic fingerprint, which may be related to increased uptake of BCAAs by the muscles, increased gluconeogenesis, and raised consumption of BCAAs.
Thus, in acromegaly, a tailored diet is a further strategy that may contribute to blunt GH/IGF-I secretion. Indeed, some authors recently suggested that "personalized" or "precision" nutrition in some conditions and diseases could have an impact on their phenotype, combining dietary recommendations with individual's genetic makeup, metabolic and microbiome characteristics, and environment. However, studies on precision nutrition in acromegaly are still in a neonatal era.
Recruitment & Eligibility
- Status
- NOT_YET_RECRUITING
- Sex
- All
- Target Recruitment
- 12
- Age 18/65
- Diagnosis of Acromegaly
- In therapy with somatostatin analogues
- pregnancy or lactation
- alchool or drugs abuse
- cancer
- Hematological diseases
Study & Design
- Study Type
- INTERVENTIONAL
- Study Design
- SINGLE_GROUP
- Arm && Interventions
Group Intervention Description Acromegalic adult in therapy with somatostatin analogues Usual clinical practice + hypoproteic diet Patients will continue the usual medical outpatient visits cadency and will keep the same pharmacological therapy throughout the whole duration of the study. Drugs have to include somatostatin analogues. At the same time, patients will be trained by an expert dietician in the habit of an isocaloric and hypoproteic diet and will come back at 2,4,6 and 8 weeks after T0 for all the necessary study assessments and compliance checking.
- Primary Outcome Measures
Name Time Method Change in disease related hormones Change from Baseline GH, IGF-1, IGFBP1, IGFBP3 blood levels at 15 days, 30 days, 45 days, 60 days Variation of GH, IGF-1, IGFBP1, IGFBP3 hormones
- Secondary Outcome Measures
Name Time Method Change in weight Change from Baseline BMI at 15 days, 30 days, 45 days, 60 days Variation of body weight assessed through body mass index change (BMI)(kg/m2)
Change in body circumferences Change from Baseline circumferences at 15 days, 30 days, 45 dyas, 60 days Variation of body circumferences (waist, hips)
Change in metabolic control Change from Baseline lipid profile at 60 days Change of cardio-metabolic risk factors: insulin resistance (HOMA-IR)
Change in kidney profile Change from Baseline Serum Creatinin at 15 days, 30 days, 45 days, 60 days Variation of serum creatinin
Change in liver profile Change from Baseline Serum Creatinin at 15 days, 30 days, 45 days, 60 days Variation of liver markers(AST, ALT, GGT)
Change in uric acid Change from Baseline uric acid in blood at 15 days, 30 days, 45 days, 60 days Variation of uric acid in blood through enzymatic determination
Change in body composition Change from Baseline fat mass% at 60 days Change of body composition (fat mass %) (DXA)
Change in blood count Change from Baseline blood count at 15 days, 30 days, 45 days, 60 days Variation of blood count
Change in microbiota Change from Baseline of prevalence of microbiota phyla at 15, 30 days, 45 days, 60 days Variation of prevalence of microbiota phyla through DNA sequencing of stools
Change in basal metabolic rate Change from Baseline basal metabolic rate at 60 days Variation of basal metabolic rate (kcal)
Change in omics profile Change from Baseline omic profile of stools at 15, 30 days, 45 days, 60 days Variation of proteomic profile of stools through liquid and gas chromatography
Change in microvesicles Change from Baseline microvesicles levels s at 15, 30 days, 45 days, 60 days Variation of serum microvesicles levels
Trial Locations
- Locations (1)
: Italy Pediatric Endocrine Service of AOU Maggiore della Carità of Novara; SCDU of Pediatrics, Department of Health Sciences, University of Eastern Piedmont
🇮🇹Novara, Italy