{"doi":"10.1111/dom.16563","title":"Reduced prandial insulin secretion contributes to prandial hyperglycaemia in non‐diabetic individuals with spinal cord injury","abstract":"Spinal cord injury (SCI), affecting ~2 million Americans with an incidence of 18 000 new injuries per year,1 is a devastating condition with deleterious effects on many body functions and structures, including autonomic dysfunction and skeletal muscle atrophy. Persons with SCI develop type 2 diabetes mellitus (T2D) at a higher rate than able-bodied (AB) individuals.2 It has long been recognized that SCI causes skeletal muscle atrophy and visceral adiposity, which in turn impairs peripheral glucose disposal by a reduction in insulin action, leading to hyperglycaemia.3 However, approximately half of diabetic patients with SCI have hyperglycaemia in the fed state with normal fasting glucose.4 Further, insulin sensitivity measured using a euglycaemic hyperinsulinaemic clamp in hyperglycaemic persons with SCI does not appear to differ from that in their normal glucose tolerant AB siblings.5 These observations suggest that in addition to abnormal insulin action, impaired prandial insulin secretion also plays a role in impaired glucose tolerance in this population. However, detailed study is lacking. Therefore, we compared plasma glucose and islet-hormone secretion in the fasting and prandial state among non-diabetic persons with and without SCI. Thirteen non-diabetic participants with SCI and eight age- and HbA1c-matched able-bodied (AB) individuals were studied (Table 1). All participants had a HbA1c below 5.8%, and were free of renal dysfunction or liver disorder. The Institutional Review Board of the University of Texas Health at San Antonio (UTHSA) approved the protocol (HSC20180070H) and AB participants provided written informed consent before participation. For SCI participants, we used the data from a similar MTT protocol that had been conducted as part of routine care and considered exempt from IRB regulation under “DHHS regulation 45 CR Category 4 (iii): secondary research uses of identifiable private information.” All subjects were instructed to not limit carbohydrates intake and not to engage in vigorous physical activity for 3 days prior to MTT. Studies were performed in the morning after an overnight fast. Supine waist circumference was measured in duplicate using an inelastic polyfibre tape measure, and body weight was measured using an adapted scale. Intravenous catheters were placed in one forearm that was used for the blood withdrawal and continuously warmed using a heating pad to arterialize the venous blood. After fasting blood samples were collected, subjects consumed a 237-mL liquid mixed meal (350 kcal; 57% carbohydrate, 15% protein and 28% fat; Ensure Plus) within 10 min. Blood samples were obtained at regular intervals for 180 min, and plasma was separated within 60 min for storage at −80°C or assayed immediately. Plasma glucose concentration was determined using an Analox GM9 Glucose Analyser. Insulin, c-peptide and glucagon concentrations were determined by enzyme-linked immunoassays (Roche Cobas E801). Haemoglobin A1c was assessed using a Roche Cobas c513. Data are presented as mean ± SEM. The parameters of interest were compared using independent Student t tests. Statistical analyses were performed using SPSS 29, and statistical significance was accepted at p < 0.05. The calculations of the glycaemic indices are described in Supplementary Appendix S1. Persons with and without SCI were similar in age and HbA1c, but 12 of 13 SCI participants were male compared with 2 out of 8 AB individuals (Table 1). Those with SCI tended to have a lower BMI (p = 0.097) despite a larger waist circumference (p = 0.001). The level of SCI ranged from C3 to T12, with 8 having paraplegia and 5 tetraplegia. A total of 12 out of the 13 participants with SCI had a motor complete injury (ASIA scores – a measure of spinal lesion completeness: A = 9, B = 3 D = 1). Fasting glucose concentration was similar between both groups (Figure 1, Table 1). Following meal ingestion, glucose concentrations increased similarly to peak concentratio","journal":"Diabetes Obesity and Metabolism","year":2025,"id":545109,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":1,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9587,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2025-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1435516,"name":"Sven P. Hoekstra","orcid":"0000-0003-1597-162X","position":1,"is_corresponding":false},{"id":476977,"name":"Amalia Gastaldelli","orcid":"0000-0003-2594-1651","position":2,"is_corresponding":false},{"id":801085,"name":"Marzieh Salehi","orcid":"0000-0003-4764-739X","position":0,"is_corresponding":true}],"reference_count":12,"raw_metadata":null,"created_at":"2026-07-19T02:53:17.418915Z","pmid":"40605147","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}