Technical note: Comparison of 3 methods for analyzing areas under the curve for glucose and nonesterified fatty acids concentrations following epinephrine challenge in dairy cows

Cardoso, F.C.; Sears, William; LeBlanc, S.J.; Drackley, J.K.

doi:10.3168/jds.2011-4627

Cited by 53 publications

(43 citation statements)

References 6 publications

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“…Long‐term fasting test, glucose tolerance test (GTT), and insulin tolerance test (ITT) were performed at 9, 10, and 11 weeks, respectively, according to the protocol . The total area under the glucose curve was calculated by using the trapezoidal method . The homeostasis model assessment for insulin resistance (HOMA‐IR) was determined by using the formula: HOMA‐IR = fasting blood glucose levels (mmol/L) × fasting blood insulin levels (mIU/L)/22.5 .…”

Section: Methodsmentioning

confidence: 99%

“…11 The total area under the glucose curve was calculated by using the trapezoidal method. 12 The homeostasis model assessment for insulin resistance (HOMA-IR) was determined by using the formula: HOMA-IR = fasting blood glucose levels (mmol/L) × fasting blood insulin levels (mIU/L)/22.5. 13 Animals were killed at the 12th week in either a fasted or a fed state.…”

Section: Animal Treatmentsmentioning

confidence: 99%

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The tacrolimus-induced glucose homeostasis imbalance in terms of the liver: From bench to bedside

Ling

Huang

Han

et al. 2020

American Journal of Transplantation

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Tacrolimus (TAC), the mainstay of maintenance immunosuppressive agents, plays a crucial role in new‐onset diabetes after transplant (NODAT). Previous studies investigating the diabetogenic effects of TAC have focused on the β cells of islets. In this study, we found that TAC contributed to NODAT through directly affecting hepatic metabolic homeostasis. In mice, TAC‐induced hypoglycemia rather than hyperglycemia during starvation via suppressing gluconeogenetic genes, suggesting the limitation of fasting blood glucose in the diagnosis of NODAT. In addition, TAC caused hepatic insulin resistance and triglyceride accumulation through insulin receptor substrate (IRS)2/AKT and sterol regulatory element binding protein (SREBP1) signaling, respectively. Furthermore, we found a pivotal role of CREB‐regulated transcription coactivator 2 (CRTC2) in TAC‐induced metabolic disorders. The restoration of hepatic CRTC2 alleviated the metabolic disorders through its downstream molecules (eg, PCK1, IRS2, and SREBP1). Consistent with the findings from bench, low CRTC2 expression in graft hepatocytes was an independent risk factor for NODAT (odds ratio = 2.692, P = .023, n = 135). Integrating grafts’ CRTC2 score into the clinical model could significantly increase the predictive capacity (areas under the receiver operating characteristic curve: 0.71 vs 0.79, P = .048). Taken together, in addition to its impact on pancreatic cells, TAC induces “hematogenous diabetes” via CRTC2 signaling. Liver‐targeted management may be of help to prevent or heal TAC‐associated diabetes.

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Section: Methodsmentioning

confidence: 99%

Section: Animal Treatmentsmentioning

confidence: 99%

The tacrolimus-induced glucose homeostasis imbalance in terms of the liver: From bench to bedside

Ling

Huang

Han

et al. 2020

American Journal of Transplantation

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“…The area under the curve (AUC) was 3 calculated for both NEFA and BHBA concentrations using the trapezoidal rule as described by Cardoso et al (2011). If an individual cow was missing more than one-third of the variables, data for that cow were eliminated from the data set before analysis.…”

Section: Discussionmentioning

confidence: 99%

Associations between hepatic metabolism of propionate and palmitate in liver slices from transition dairy cows

McCarthy

Piepenbrink

Overton

2015

Journal of Dairy Science

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Multiparous Holstein cows (n=95) were used to evaluate changes in hepatic propionate and palmitate metabolism and liver composition over time during the transition period, along with the relationships of these variables with cumulative increases in nonesterified fatty acids and β-hydroxybutyrate during the periparturient period. Data from 3 previous experiments were used to address the study objectives, accounting for a total of 95 multiparous Holstein cows. Liver slices from biopsies on d -21, 1, and 21 relative to parturition were used to determine conversion of [1-(14)C]palmitate to CO2 and esterified products (EP) and the conversion of [1-(14)C]propionate to CO2 and glucose. Hepatic glycogen content was highest on d -21 and was 26.9 and 36.5% of prepartum values on d 1 and 21, respectively. Liver triglyceride content was lowest at d -21 and was 271 and 446% of prepartum values on d 1 and 21, respectively. We detected no difference in the capacity for the liver to oxidize [1-(14)C]palmitate to CO2 between d -21 and d 1; however, on d 21, oxidation was 84% of prepartum values. The capacity of the liver to convert [1-(14)C]palmitate to EP was 148 and 139% of prepartum values on d 1 and 21, respectively. The capacity of liver to convert [1-(14)C]propionate to CO2 was 127 and 83% of prepartum values on d 1 and 21, and the capacity of liver to convert [1-(14)C]propionate to glucose was 126 and 85% of prepartum values on d 1 and 21, respectively. Correlation relationships suggest that overall, cows with elevated prepartum liver triglyceride content had elevated triglycerides throughout the transition period along with increased [1-(14)C]palmitate oxidation and conversion to EP and a decreased propensity to convert [1-(14)C]propionate to glucose. Cows with increased [1-(14)C]propionate oxidation had increased conversion of [1-(14)C]propionate to glucose throughout the transition period. Overall, conditions that lead to impairments in fatty acid metabolism during the transition period appear to be associated with impaired postpartum hepatic propionate metabolism.

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“…Mice were injected with d -glucose (20% in saline, ip) or human insulin (Novolin, 0.0125 µM/g body weight, ip) and blood glucose was quantified at 0–120 min. Total area under the curve (AUC; arbitrary units), which is obtained without the presence of a baseline, calculates the area below the observed concentrations and, in comparison studies, was reported to compare favorably to the positive incremental area method for statistical analyses of glucose tolerance data (Cardoso et al 2011). …”

Section: Methodsmentioning

confidence: 99%

Coplanar Polychlorinated Biphenyls Impair Glucose Homeostasis in Lean C57BL/6 Mice and Mitigate Beneficial Effects of Weight Loss on Glucose Homeostasis in Obese Mice

Baker

Karounos²,

English³

et al. 2013

Environ Health Perspect

108

119

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Background: Previous studies demonstrated that coplanar polychlorinated biphenyls (PCBs) promote proinflammatory gene expression in adipocytes. PCBs are highly lipophilic and accumulate in adipose tissue, a site of insulin resistance in persons with type 2 diabetes.Objectives: We investigated the in vitro and in vivo effects of coplanar PCBs on adipose expression of tumor necrosis factor α (TNF-α) and on glucose and insulin homeostasis in lean and obese mice.Methods: We quantified glucose and insulin tolerance, as well as TNF-α levels, in liver, muscle, and adipose tissue of male C57BL/6 mice administered vehicle, PCB-77, or PCB-126 and fed a low fat (LF) diet. Another group of mice administered vehicle or PCB-77 were fed a high fat (HF) diet for 12 weeks; the diet was then switched from HF to LF for 4 weeks to induce weight loss. We quantified glucose and insulin tolerance and adipose TNF-α expression in these mice. In addition, we used in vitro and in vivo studies to quantify aryl hydrocarbon receptor (AhR)-dependent effects of PCB-77 on parameters of glucose homeostasis.Results: Treatment with coplanar PCBs resulted in sustained impairment of glucose and insulin tolerance in mice fed the LF diet. In PCB-77–treated mice, TNF-α expression was increased in adipose tissue but not in liver or muscle. PCB-77 levels were strikingly higher in adipose tissue than in liver or serum. Antagonism of AhR abolished both in vitro and in vivo effects of PCB-77. In obese mice, PCB-77 had no effect on glucose homeostasis, but glucose homeostasis was impaired after weight loss.Conclusions: Coplanar PCBs impaired glucose homeostasis in lean mice and in obese mice following weight loss. Adipose-specific elevations in TNF-α expression by PCBs may contribute to impaired glucose homeostasis.

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Technical note: Comparison of 3 methods for analyzing areas under the curve for glucose and nonesterified fatty acids concentrations following epinephrine challenge in dairy cows

Cited by 53 publications

References 6 publications

The tacrolimus-induced glucose homeostasis imbalance in terms of the liver: From bench to bedside

The tacrolimus-induced glucose homeostasis imbalance in terms of the liver: From bench to bedside

Associations between hepatic metabolism of propionate and palmitate in liver slices from transition dairy cows

Coplanar Polychlorinated Biphenyls Impair Glucose Homeostasis in Lean C57BL/6 Mice and Mitigate Beneficial Effects of Weight Loss on Glucose Homeostasis in Obese Mice

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