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. 2024 Sep 18;38(6):3309–3314. doi: 10.1111/jvim.17199

Value of measuring markers of lipid metabolism in horses during an oral glucose test

Claire H K Zemek 1, Kate L Kemp 1, François‐René Bertin 1,2,✉
PMCID: PMC11586554  PMID: 39291576

Abstract

Background

Characterizing the lipid response to an oral glucose test (OGT) might improve our understanding of Equine Metabolic Syndrome.

Hypothesis/Objectives

To describe the effects of an OGT on lipid metabolism and determine the value of measuring triglyceride and nonesterified fatty acid (NEFA) concentrations in hyperinsulinemic (HI) and insulin‐resistant (IR) horses.

Animals

Twenty horses including 7 HI‐IR horses, 4 HI‐non‐IR horses, and 9 non‐HI‐non‐IR horses (control).

Methods

Cross‐sectional design. Horses underwent an OGT, with blood samples collected at 0, 60, 90, and 120 minutes. Insulin, glucose, triglyceride, and NEFA concentrations were measured and compared over time and between groups, with P < .05 considered significant.

Results

In all horses, the OGT had a significant effect on triglyceride concentrations (median [interquartile range]: .35 [.30‐.50] mmol/L at 0 minute vs .25 [.21‐.37] mmol/L at 120 minutes, P = .005) and on NEFA concentrations (.1 [.1‐.2] mEq/L at 0 minute vs .05 [.05‐.1] mEq/L at 120 minutes, P = .0009). However, horses with HI and IR had higher triglyceride areas under the curve (AUC, 79.46 ± 46.59 vs 33.32 ± 6.75 mmol/L*min, P = .01) as well as NEFA AUC (9.1 ± 2.9 vs 6.0 ± 6.8 mEq/L*min, P = .03) than control horses. No significant difference was detected between control and HI non‐IR horses.

Conclusions and Clinical Importance

Determining triglyceride and NEFA concentrations might help assess tissue insulin resistance during an OGT.

Keywords: endocrinology, equine metabolic syndrome, insulin dysregulation, insulin resistance, nonesterified fatty acids, triglycerides

Abbreviations

AUC

area under the curve

BCS

body condition score

CNS

cresty neck score

EMS

Equine Metabolic Syndrome

HI‐IR

hyperinsulinemic and insulin‐resistant

HI‐NIR

hyperinsulinemic and noninsulin‐resistant

ID

insulin dysregulation

IR

insulin‐resistant

mFSIGTT

modified frequently sampled IV glucose tolerance test

NEFA

nonesterified fatty acid

OGT

oral glucose test

1. INTRODUCTION

Insulin dysregulation (ID) manifests as either hyperinsulinemia (resting or in response to a carbohydrate challenge), tissue insulin resistance, or a combination of those conditions. 1 Due to hyperinsulinemia being directly associated with the development of laminitis, detection of hyperinsulinemia has been the focus of most diagnostic tests in practice, often by testing resting serum insulin concentrations or using an oral sugar test or oral glucose test (OGT). 2 , 3 Tissue insulin resistance is comparably more challenging to assess and therefore often neglected in equine practice, due to the technical complexity associated with the euglycemic hyperinsulinemic clamp or the risk of inducing hypoglycemia with the 2‐step insulin tolerance test. 4 , 5 In other species, tissue insulin resistance is considered the central component of glucose metabolism disorders and is associated with morphometric changes and the development of obesity. 6 In horses, measures such as body condition score (BCS) and cresty neck score (CNS) have been used as proxies of obesity and to some extent tissue insulin resistance before the concept of equine ID was adopted. 7 , 8 , 9 As there are lean horses with ID and metabolically healthy obese horses, the association between obesity and ID and its different components has been inconsistent, and obesity is now considered an exacerbating factor rather than a cause of ID. 10 , 11 , 12 , 13 Despite inconsistent associations, adipose tissue is recognized as an endocrine tissue of interest with storage of fat and release of adipokines, such as leptin and adiponectin, involved in appetite regulation, energy expenditure, and modulation of inflammation. 10 , 12 This suggests that a better assessment of lipid metabolism in horses with ID might improve our understanding of the different elements of Equine Metabolic Syndrome (EMS) and management of affected horses.

Triglycerides and nonesterified fatty acids (NEFA) can be indicators of a horse's lipidemic status with both now able to be measured through affordable and stall‐side assays from serum samples making them relevant targets in the evaluation of horses with or at risk of EMS. Changes in triglyceride and NEFA concentrations have been documented previously in the context of changes in diet, body condition, inflammatory states, and ID status in ponies and horses. 7 , 13 , 14 , 15 Equine Metabolic Syndrome might be associated with higher basal serum triglyceride concentrations, but this has not been consistently demonstrated, even in large‐scale studies. 9 , 16 , 17 , 18 , 19 , 20 , 21 , 22 Lipid responses to blood insulin changes induced by an enteric glucose challenge are not well understood in horses with different components of ID. Evaluating triglyceride and NEFA concentrations of horses during an OGT might create a more complete picture of the extent or severity of an individual's ID. The aim of this study was therefore to investigate how an acute and transient carbohydrate‐induced increase in insulin concentrations influences triglyceride and NEFA concentrations in horses, including HI and insulin‐resistant horses, and to evaluate if phenotypic markers of adiposity, such as BCS and CNS, are correlated with triglyceride and NEFA concentrations. We hypothesized that the hyperinsulinemic and insulin resistance status of horses with ID would mitigate the triglyceride and NEFA response to an OGT.

2. MATERIALS AND METHODS

2.1. Horses

Procedures were approved by the institutional animal ethics committee. Twenty mixed breed horses, including 8 geldings and 12 mares, were enrolled in this study in the months of November and December (Southern hemisphere). Abnormalities were not detected on physical examination of enrolled horses throughout the study. Horses were acclimatized for a week in individual dirt yards before the experiments with ad libitum access to lucerne hay and water. The hyperinsulinemic status was determined by an OGT, with horses with an insulin concentration >65 μIU/mL within 120 minutes after initiating the OGT being designated hyperinsulinemic. Horses were diagnosed as insulin‐resistant based on the insulin sensitivity index, calculated after a modified frequently sampled IV glucose tolerance test (mFSIGTT), being <1.0 × 10−4 L/mIU/min, as previously described. 4 Complete insulin and glucose data for the OGT and the mFSIGTT have been presented elsewhere and the mFSIGTT was preferred over the 2‐step insulin tolerance test as it offers a more complete assessment of insulin sensitivity. 23 To investigate the effect of ID on triglyceride and NEFA concentrations, horses were initially divided into ID vs control horses with ID defined as being either hyperinuslinemic or insulin‐resistant. Then, to investigate, the differential effect of hyperinsulinemia (resting or after a carbohydrate challenge) and tissue insulin resistance, horses were further divided into 3 groups: both hyperinsulinemic and insulin‐resistant (HI‐IR), hyperinsulinemic but not insulin‐resistant (HI‐NIR), and neither hyperinsulinemic nor insulin‐resistant (control horses). Breed, age, sex, body weight, BCS (using the Henneke's system), and CNS (using the Carter's system) were recorded for each horse. 8 , 9

2.2. Oral glucose test

Feed was withheld for 10 hours before the OGT to avoid measurements being confounded by recent feed consumption, and IV catheters were aseptically placed into the left jugular vein for blood sample collection. 24 Baseline blood samples (0 minute) were obtained after discarding the first 5 mL of blood into a syringe, then drawing the sample for analysis into a serum tube (BD Vacutainer Serum Tube, Becton Dickinson, Sydney, New South Wales). Nasogastric intubation was used to ensure the accurate and timely delivery of the .75 g/kg dextrose dose dissolved in 2 L of warm water. 25 Timing was started once the nasogastric tube was removed and samples were collected at 60, 90, and 120 minutes via the same method as for the 0 minute sample.

2.3. Biochemical assays

Glucose concentrations were measured on whole blood using a handheld glucometer (AlphaTRAK, Zoetis, Sydney, New South Wales). 26 The remaining analytes were measured in serum samples with blood samples collected in serum tubes, allowed to clot at room temperature, and centrifuged at 1370 g for 10 minutes. Serum was pipetted into cryotubes (Eppendorf Tubes, Eppendorf South Pacific, Sydney, New South Wales) and stored until analysis at −80°C. To measure insulin concentrations, the previously validated chemiluminescent assay (Immulite 1000 Immunoassay System, Siemens Healthineers, Melbourne, Victoria) was used. 27 When the insulin concentrations > 300 μIU/mL, dilution was undertaken using the manufacturer diluent (Item no. 10387034, Siemens Healthineers, Melbourne, Victoria, Australia) at a 1:1 ratio with 150 μL of serum and diluent. Triglyceride and NEFA concentrations were determined on a commercial biochemical analyzer (AU480 Chemistry Analyzer, Beckman Coulter Australia, Sydney, New South Wales, Australia). 16 , 17

2.4. Statistical analyses

Data were analyzed using GraphPad Prism v. 10.1.0 (GraphPad Software, LLC, Boston, Massachusetts, USA). Normality of continuous variables was evaluated using the Shapiro‐Wilk test. Normally distributed data were presented as mean ± SD, and not normally distributed data were presented as median (interquartile range). The area under the curve (AUC) was calculated using the trapezoid method for all horses' triglyceride‐time and NEFA‐time graphs using 0 as baseline. Mann‐Whitney, 1‐way or 2‐way analyses of variance with Tukey's or Šidák's multiple comparisons were used to compare triglycerides, NEFA concentrations, or AUC among groups and over time, and to compare BCS and CNS among groups. One‐variable linear regressions were used to determine associations of triglyceride and NEFA concentrations with BCS and CNS. The statistical significance was based on a P value <.05.

3. RESULTS

All horses tolerated the experimental procedures without complications. Based on the OGT and mFSIGTT results, 11 horses were considered hyperinsulinemic, of which 7 were also insulin‐resistant, and the remaining 9 were neither hyperinsulinemic nor insulin‐resistant leaving the following comparisons: ID (n = 11) vs control horses (n = 9) and HI‐IR (n = 7) vs. HI‐NIR (n = 4) vs control horses (n = 9). Details about horses are presented in Table S1.

3.1. Triglycerides

In both horses with ID and control horses, oral dextrose administration resulted in a significant decrease in triglyceride concentrations (P < .001), though horses with ID had significantly higher triglyceride concentrations (P = .03) and AUC (45.60 [35.25‐86.85] vs 35.55 [26.63‐38.70] mmol/L*min, P = .02) than the control horses.

Similarly, in HI‐IR, HI‐NIR, and control horses, oral dextrose administration resulted in a significant decrease in triglyceride concentrations (P < .001, Figure 1); however, only horses with tissue insulin resistance had significantly higher triglyceride concentrations (P = .02) and AUC (79.46 ± 46.59 vs 33.32 ± 6.75 mmol/L*min, P = .01) than control horses. No significant difference was detected between control horses and horses with only hyperinsulinemia.

FIGURE 1.

FIGURE 1

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Triglyceride concentrations in control horses (n = 9) vs hyperinsulinemic and noninsulin‐resistant horses (HI‐NIR, n = 4) vs hyperinsulinemic and insulin‐resistant horses (HI‐IR, n = 7). *P < .05, **P < .01.

3.2. Nonesterified fatty acids

In both horses with ID and control horses, oral dextrose administration resulted in a significant decrease in NEFA concentrations (P < .001). Horses with ID had significantly higher NEFA concentrations (P = .04) and AUC (12.0 [9.8‐15.0] vs 9.0 [6.0‐12.4] mEq/L*min, P = .04) than control horses; however, this was only detected at 60 minutes (.12 ± .07 vs .07 ± .03, P = .02).

In the HI‐IR, HI‐NIR and control horses, oral dextrose administration also resulted in a significant decrease in NEFA concentrations (P = .02, Figure 2) with only horses with tissue insulin resistance having higher NEFA concentrations (P = .02) and AUC (9.1 ± 2.9 vs 6.0 ± 6.8 mEq/L*min, P = .03) than the control horses; again, this was only detected at 60 minutes (.14 ± .08 vs .07 ± .03, P = .007). No significant difference was detected between control horses and horses with only hyperinsulinemia.

FIGURE 2.

FIGURE 2

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Nonesterified fatty acid concentrations in control horses (n = 9) vs hyperinsulinemic and noninsulin‐resistant horses (HI‐NIR, n = 4) vs hyperinsulinemic and insulin‐resistant horses (HI‐IR, n = 7). **P < .01.

3.3. Morphometric measurements

There was a significant group effect on BCS with control horses (5/9 [5‐5]) having a significantly lower BCS than HI horses regardless of the tissue insulin resistance status (HI‐NIR horses, 7/9 [5‐8], P = .001; and HI‐IR horses, 8/9 [7‐8], P < .001). There was a weak yet significant positive association between BCS and triglyceride AUC (r2 = .23, P = .03) and NEFA AUC (r2 = .38, P = .004).

There was also a significant group effect on CNS with horses with tissue insulin resistance (3/5 [3‐4]) having a significantly higher CNS than insulin‐sensitive horses, regardless of the HI status (HI‐NIR horses, 3/5 [2‐3], P = .04; and control horses, 2/5 [2‐2], P < .001). There was a significant positive association between CNS and triglyceride AUC (r2 = .32, P = .009) and NEFA AUC (r2 = .32, P = .01).

4. DISCUSSION

The results of this study suggest that acute increases in insulin concentration induced by carbohydrate intake lead to a decrease in triglyceride and NEFA concentrations in horses, and fat mobilization and accumulation differ between horses exhibiting different components of ID.

Beyond its role in glucose metabolism, insulin plays a pivotal role in lipid metabolism with high concentrations inhibiting hormone‐sensitive lipase, thereby reducing triglyceride mobilization from adipocytes and promoting tissue uptake and use of triglycerides and NEFA through stimulation of lipoprotein lipases. 7 , 14 , 28 , 29 On the other hand, when glucose becomes scarce, low insulin concentrations allow for increased hormone‐sensitive lipase activity resulting in the release of triglycerides and NEFA that can be used for energy production. 30 , 31 This is consistent with our findings; in both control horses and horses with ID, increasing concentrations of insulin decreased circulating triglyceride and NEFA concentrations, indicating that all horses were sensitive to insulin's effects on lipid metabolism to some degree.

The association between ID and lipid metabolism has been extensively investigated, although consensus remains elusive. In our study, although all horses exhibited a decrease in triglyceride and NEFA concentrations after dextrose administration, this decrease was less pronounced in horses with ID. This would be consistent with previous studies that found that horses with ID have higher triglyceride and NEFA concentrations. 10 , 18 When investigating the different arms of ID, however, only horses with tissue insulin resistance had a blunted triglyceride and NEFA response to insulin while horses that were only hyperinsulinemic did not. Various diagnostic methods have been used in previous studies to investigate the association between triglyceride or NEFA concentrations and ID; however, the varying sensitivities, specificities, and endpoints of these tests can make comparisons between studies challenging. 32 In studies defining ID by measuring resting insulin concentrations, high insulin concentrations were associated with high triglyceride concentrations. 17 , 21 Similar findings were described in studies defining ID by measuring insulin concentrations after an oral sugar test. 18 The results obtained in that study were obtained in large cohorts of ponies and would be in contradiction with ours in which horses with ID defined as hyperinsulinemi, either by resting insulin concentration or OGT, did not have higher triglyceride or NEFA concentrations and increasing concentrations of insulin failed to alter triglyceride and NEFA concentrations. A possible explanation for this discrepancy includes our low sample size that could have prevented us from detecting a significant difference. However, in other studies that defined ID by measuring tissue insulin sensitivity, resting triglycerides concentrations were associated with insulin resistance, and increased insulin sensitivity was associated with lower triglycerides and NEFA concentrations. 10 , 33 Therefore, as different diagnostic approaches capture different arms of ID, it is possible that different lipid responses could reflect different subpopulations of insulin and glucose disorders, like in other species. In diabetes and obesity research, the primary focus has been on tissue insulin resistance rather than hyperinsulinemia. It has been demonstrated that lipid metabolites can impair insulin signaling directly by down‐regulating lipid and fatty acid transporters in insulin‐sensitive tissues. Indirectly, these metabolites contribute to tissue insulin resistance through mechanisms such as crosstalk between inflammatory and insulin signaling pathways, mitochondrial dysfunction, and oxidative stress. 14 , 34 , 35 This impairment is often compensated by an increase in circulating insulin concentrations. While such evidence is lacking in horses, several studies have reported the activation of inflammatory pathways with ID suggesting that similar mechanisms might exist, and that measuring markers of lipid metabolism (such as triglycerides and NEFA) during dynamic testing could help define subpopulations of horses with ID and refine our understanding of EMS. 36 , 37 , 38

In addition to lipid mobilization, our data suggest that fat storage could differ between horses with different components of ID. Cresty neck score had a positive association with triglyceride and NEFA concentrations, supporting that lipid dysregulation is associated with abnormal fat distribution characteristics of horses with a typical EMS phenotype. 9 , 39 Again, the association between adiposity and ID status has been inconsistently reported in the literature, and the role of obesity in the development of ID has been reconsidered. 13 In our study, the presence of tissue insulin resistance was associated with an increased regional adiposity and CNS, with insulin‐resistant horses exhibiting significantly higher scores compared to control horses and only hyperinsulinemic horses. In another study, CNS was found to be an independent predictor of ID defined as an increased response to an OGT; however, no information on insulin sensitivity was provided, making comparison difficult. 39 Considering that no pony was hypoglycemic in that study, and that ponies have a lower insulin sensitivity, a degree of tissue insulin resistance could be present and one could assume those ponies would have been considered as HI‐IR in our study. 40 Another possible explanation for the differences between that study and ours is the difference between horses and ponies; our study only enrolled horses while the other study only included ponies. Horses with a high CNS are not more likely to be hyperinsulinemic while ponies with a high CNS are almost 19 times more likely to be hyperinsulinemic. 9

Body condition was higher in hyperinsulinemic horses than in control horses, regardless of the insulin resistance status, and there was a weak yet significant association between BCS and triglycerides and NEFA concentrations. This finding is consistent with a previous study on a large cohort of horses and ponies where higher BCS were associated with higher insulin and triglyceride concentrations. 11 This association is, however, not consistent across the literature, as several studies found no associations between high, or increasing, BCS and triglyceride or NEFA concentrations. 16 , 39 , 41 In addition, assessments of insulin sensitivity in horses gaining weight have produced conflicting results regarding the associations between tissue insulin resistance, triglyceride and NEFA concentrations, and BCS. 7 , 12 , 42 This supports that generalized obesity would be an exacerbating factor rather than a central component of EMS and that a better characterization of horses and ponies with ID might improve our understanding of the role of lipids in this condition.

Several limitations to this study should be acknowledged, including the small experimental sample size, especially when horses were divided into control, HI‐NIR, and HI‐IR horses. A larger sample size might have allowed statistical significance to be attained in more comparisons between these groups and in interactions between those variables. While the OGT and mFSIGTT distinguished HI‐NIR and HI‐IR horses, there were no insulin‐resistant but not hyperinsulinemic horses among the study sample. This would have been insightful to determine if hyperinsulinemia is necessary for insulin‐resistant horses to have higher triglycerides and NEFA, or if tissue insulin resistance alone is sufficient. In addition, hyperinsulinemic horses included horses with resting hyperinsulinemia and horses with hyperinsulinemia after the OGT. While the clinical outcome of interest is the insulin concentration and the risk of laminitis, the pathophysiological mechanisms between those 2 phenotypes likely differ and separate analyses might have been warranted if a larger sample size had been reached. A larger range in BCS and CNS would have also allowed a better documentation of the lean EMS phenotype. As this study only evaluated insulin, glucose, triglycerides, and NEFA concentrations, other major mediators of glucose and lipid metabolism, in particular glucagon, somatostatin, incretins, and adipokines, are having known effects on these analytes and would have helped with the interpretation of the observed changes. 12 While our study controlled for diet in the immediate peri‐experimental period, long‐term effects of an uncontrolled diet before the experiment were not considered. 13 , 28 Additionally, breed, which influences individual predisposition to ID, was not controlled for; however, the diverse study sample might enhance clinical applicability. 40

Overall, triglycerides and NEFA concentrations decreased during the OGT; however, this decrease was blunted by the presence of tissue insulin resistance. As triglycerides and NEFA assays are becoming readily accessible to equine practitioners, including stall‐side analytical platforms, measuring these concentrations, alongside insulin during an OGT, could offer insights into the horse's insulin and lipid regulation status, particularly in detecting tissue insulin resistance in hyperinsulinemic horses. Furthermore, our results underscore phenotypic differences between horses with hyperinsulinemia alone and those with hyperinsulinemia and tissue insulin resistance, highlighting the existence of distinct subpopulations within the ID and EMS diagnoses.

CONFLICT OF INTEREST DECLARATION

Authors declare no conflict of interest.

OFF‐LABEL ANTIMICROBIAL DECLARATION

Authors declare no off‐label use of antimicrobials.

INSTITUTIONAL ANIMAL CARE AND USE COMMITTEE (IACUC) OR OTHER APPROVAL DECLARATION

Approved by The University of Queensland Animal Ethics Committee (No. SVS/153/19).

HUMAN ETHICS APPROVAL DECLARATION

Authors declare human ethics approval was not needed for this study.

Supporting information

Table S1. Horse data displayed by group, based on their hyperinsulinemic and insulin resistance status. Normally distributed data are presented as mean ± SD, not‐normally distributed data are presented as median (range).

JVIM-38-3309-s001.docx (18.8KB, docx)

ACKNOWLEDGMENTS

Funding was provided by the Morris Animal Foundation (D19‐EQ‐302) and The University of Queensland School of Veterinary Science (VETS5017). Open access publishing facilitated by The University of Queensland, as part of the Wiley ‐ The University of Queensland agreement via the Council of Australian University Librarians.

Zemek CHK, Kemp KL, Bertin F‐R. Value of measuring markers of lipid metabolism in horses during an oral glucose test. J Vet Intern Med. 2024;38(6):3309‐3314. doi: 10.1111/jvim.17199

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Supplementary Materials

Table S1. Horse data displayed by group, based on their hyperinsulinemic and insulin resistance status. Normally distributed data are presented as mean ± SD, not‐normally distributed data are presented as median (range).

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