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  • American Diabetes Association  (11)
  • 1
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    A Type 1 Diabetes Genetic Risk Score Predicts Progression of Islet Autoimmunity and Development of Type 1 Diabetes in Individuals at Risk
    American Diabetes Association ; 2018
    In:  Diabetes Care Vol. 41, No. 9 ( 2018-09-01), p. 1887-1894
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 41, No. 9 ( 2018-09-01), p. 1887-1894
    Abstract: We tested the ability of a type 1 diabetes (T1D) genetic risk score (GRS) to predict progression of islet autoimmunity and T1D in at-risk individuals. RESEARCH DESIGN AND METHODS We studied the 1,244 TrialNet Pathway to Prevention study participants (T1D patients’ relatives without diabetes and with one or more positive autoantibodies) who were genotyped with Illumina ImmunoChip (median [range] age at initial autoantibody determination 11.1 years [1.2–51.8], 48% male, 80.5% non-Hispanic white, median follow-up 5.4 years). Of 291 participants with a single positive autoantibody at screening, 157 converted to multiple autoantibody positivity and 55 developed diabetes. Of 953 participants with multiple positive autoantibodies at screening, 419 developed diabetes. We calculated the T1D GRS from 30 T1D-associated single nucleotide polymorphisms. We used multivariable Cox regression models, time-dependent receiver operating characteristic curves, and area under the curve (AUC) measures to evaluate prognostic utility of T1D GRS, age, sex, Diabetes Prevention Trial–Type 1 (DPT-1) Risk Score, positive autoantibody number or type, HLA DR3/DR4-DQ8 status, and race/ethnicity. We used recursive partitioning analyses to identify cut points in continuous variables. RESULTS Higher T1D GRS significantly increased the rate of progression to T1D adjusting for DPT-1 Risk Score, age, number of positive autoantibodies, sex, and ethnicity (hazard ratio [HR] 1.29 for a 0.05 increase, 95% CI 1.06–1.6; P = 0.011). Progression to T1D was best predicted by a combined model with GRS, number of positive autoantibodies, DPT-1 Risk Score, and age (7-year time-integrated AUC = 0.79, 5-year AUC = 0.73). Higher GRS was significantly associated with increased progression rate from single to multiple positive autoantibodies after adjusting for age, autoantibody type, ethnicity, and sex (HR 2.27 for GRS & gt;0.295, 95% CI 1.47–3.51; P = 0.0002). CONCLUSIONS The T1D GRS independently predicts progression to T1D and improves prediction along T1D stages in autoantibody-positive relatives.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc18-0087
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
    detail.hit.zdb_id: 1490520-6
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  • 2
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    Identical and Nonidentical Twins: Risk and Factors Involved in Development of Islet Autoimmunity and Type 1 Diabetes
    American Diabetes Association ; 2019
    In:  Diabetes Care Vol. 42, No. 2 ( 2019-02-01), p. 192-199
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 42, No. 2 ( 2019-02-01), p. 192-199
    Abstract: There are variable reports of risk of concordance for progression to islet autoantibodies and type 1 diabetes in identical twins after one twin is diagnosed. We examined development of positive autoantibodies and type 1 diabetes and the effects of genetic factors and common environment on autoantibody positivity in identical twins, nonidentical twins, and full siblings. RESEARCH DESIGN AND METHODS Subjects from the TrialNet Pathway to Prevention Study (N = 48,026) were screened from 2004 to 2015 for islet autoantibodies (GAD antibody [GADA], insulinoma-associated antigen 2 [IA-2A] , and autoantibodies against insulin [IAA]). Of these subjects, 17,226 (157 identical twins, 283 nonidentical twins, and 16,786 full siblings) were followed for autoantibody positivity or type 1 diabetes for a median of 2.1 years. RESULTS At screening, identical twins were more likely to have positive GADA, IA-2A, and IAA than nonidentical twins or full siblings (all P & lt; 0.0001). Younger age, male sex, and genetic factors were significant factors for expression of IA-2A, IAA, one or more positive autoantibodies, and two or more positive autoantibodies (all P ≤ 0.03). Initially autoantibody-positive identical twins had a 69% risk of diabetes by 3 years compared with 1.5% for initially autoantibody-negative identical twins. In nonidentical twins, type 1 diabetes risk by 3 years was 72% for initially multiple autoantibody–positive, 13% for single autoantibody–positive, and 0% for initially autoantibody-negative nonidentical twins. Full siblings had a 3-year type 1 diabetes risk of 47% for multiple autoantibody–positive, 12% for single autoantibody–positive, and 0.5% for initially autoantibody-negative subjects. CONCLUSIONS Risk of type 1 diabetes at 3 years is high for initially multiple and single autoantibody–positive identical twins and multiple autoantibody–positive nonidentical twins. Genetic predisposition, age, and male sex are significant risk factors for development of positive autoantibodies in twins.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc18-0288
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
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  • 3
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    A Low-Frequency Inactivating AKT2 Variant Enriched in the Finnish Population Is Associated With Fasting Insulin Levels and Type 2 Diabetes Risk
    American Diabetes Association ; 2017
    In:  Diabetes Vol. 66, No. 7 ( 2017-07-01), p. 2019-2032
    Details
    In: Diabetes, American Diabetes Association, Vol. 66, No. 7 ( 2017-07-01), p. 2019-2032
    Abstract: To identify novel coding association signals and facilitate characterization of mechanisms influencing glycemic traits and type 2 diabetes risk, we analyzed 109,215 variants derived from exome array genotyping together with an additional 390,225 variants from exome sequence in up to 39,339 normoglycemic individuals from five ancestry groups. We identified a novel association between the coding variant (p.Pro50Thr) in AKT2 and fasting plasma insulin (FI), a gene in which rare fully penetrant mutations are causal for monogenic glycemic disorders. The low-frequency allele is associated with a 12% increase in FI levels. This variant is present at 1.1% frequency in Finns but virtually absent in individuals from other ancestries. Carriers of the FI-increasing allele had increased 2-h insulin values, decreased insulin sensitivity, and increased risk of type 2 diabetes (odds ratio 1.05). In cellular studies, the AKT2-Thr50 protein exhibited a partial loss of function. We extend the allelic spectrum for coding variants in AKT2 associated with disorders of glucose homeostasis and demonstrate bidirectional effects of variants within the pleckstrin homology domain of AKT2.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db16-1329
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2017
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  • 4
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    Relation of Lipoprotein(a) Levels to Incident Type 2 Diabetes and Modification by Alirocumab Treatment
    American Diabetes Association ; 2021
    In:  Diabetes Care Vol. 44, No. 5 ( 2021-05-01), p. 1219-1227
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 44, No. 5 ( 2021-05-01), p. 1219-1227
    Abstract: In observational data, lower levels of lipoprotein(a) have been associated with greater prevalence of type 2 diabetes. Whether pharmacologic lowering of lipoprotein(a) influences incident type 2 diabetes is unknown. We determined the relationship of lipoprotein(a) concentration with incident type 2 diabetes and effects of treatment with alirocumab, a PCSK9 inhibitor. RESEARCH DESIGN AND METHODS In the ODYSSEY OUTCOMES trial alirocumab was compared with placebo in patients with acute coronary syndrome. Incident diabetes was determined from laboratory, medication, and adverse event data. RESULTS Among 13,480 patients without diabetes at baseline, 1,324 developed type 2 diabetes over a median 2.7 years. Median baseline lipoprotein(a) was 21.9 mg/dL. With placebo, 10 mg/dL lower baseline lipoprotein(a) was associated with hazard ratio 1.04 (95% CI 1.02−1.06, P & lt; 0.001) for incident type 2 diabetes. Alirocumab reduced lipoprotein(a) by a median 23.2% with greater absolute reductions from higher baseline levels and no overall effect on incident type 2 diabetes (hazard ratio 0.95, 95% CI 0.85–1.05). At low baseline lipoprotein(a) levels, alirocumab tended to reduce incident type 2 diabetes, while at high baseline lipoprotein(a) alirocumab tended to increase incident type 2 diabetes compared with placebo (treatment–baseline lipoprotein(a) interaction P = 0.006). In the alirocumab group, a 10 mg/dL decrease in lipoprotein(a) from baseline was associated with hazard ratio 1.07 (95% CI 1.03−1.12; P = 0.0002) for incident type 2 diabetes. CONCLUSIONS In patients with acute coronary syndrome, baseline lipoprotein(a) concentration associated inversely with incident type 2 diabetes. Alirocumab had neutral overall effect on incident type 2 diabetes. However, treatment-related reductions in lipoprotein(a), more pronounced from high baseline levels, were associated with increased risk of incident type 2 diabetes. Whether these findings pertain to other therapies that reduce lipoprotein(a) is undetermined.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc20-2842
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2021
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  • 5
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    Risk Factors for Cardiovascular Disease (CVD) in Adults with Type 1 Diabetes (T1D)
    American Diabetes Association ; 2018
    In:  Diabetes Vol. 67, No. Supplement_1 ( 2018-07-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: The T1D Exchange (T1DX) Clinic Registry assessed CVD risk factors in a large, contemporary cohort of adults with T1D living in the U.S. To understand the incidence and CVD risk factors, we evaluated the association of CVD risk factors and 5-year risk of CVD in adults ≥18 years of age, without CVD at enrollment in the T1DX. CVD was defined as a composite outcome of clinic reported fatal or non-fatal events of ischemic heart disease and heart failure. Associations between diabetic specific and traditional CVD risk factors and incident CVD were examined by logistic regression adjusting for potential confounders. The study included 4,463 participants (55% female, 91% non-Hispanic white, mean age 41 years, T1D duration 21 years). At enrollment, mean HbA1c was 7.7%, 43% used statin, and 45% used blood pressure medication. Incident CVD was reported by 419 (9.4%) participants during the 5-year follow-up. Age, diabetes duration, elevated BMI, triglycerides (TG), and diabetic nephropathy were associated with greater odds of CVD [Table]. Sex, mean HbA1c, HbA1c variability, pulse pressure, and hypertension were not associated with CVD. Markers of insulin resistance (BMI and TG) and diabetic nephropathy are important risk factors for CVD. Longer follow-up is required to assess the impact of other CVD risk factors on CVD in adults with T1D. Disclosure S.N. Mehta: None. M. Wu: None. N.C. Foster: None. R. Pop-Busui: Research Support; Self; AstraZeneca. M. Katz: None. J.P. Crandall: None. F. Bacha: Research Support; Self; AstraZeneca, JAEB Center For Health Research, National Institutes of Health, Pediatric Diabetes Consortium. K.J. Nadeau: None. I. Libman: Consultant; Self; Novo Nordisk A/S. P. Hiers: None. K.R. Mizokami-Stout: None. L. DiMeglio: Advisory Panel; Self; Eli Lilly and Company. Research Support; Self; Dexcom, Inc., Medtronic, Sanofi, Caladrius Biosciences, Inc., Janssen Research & Development, Xeris Pharmaceuticals, Inc., Sanofi. J. Sherr: Consultant; Self; Medtronic MiniMed, Inc.. Advisory Panel; Self; Insulet Corporation, Eli Lilly and Company, Bigfoot Biomedical. R.E. Pratley: Other Relationship; Self; AstraZeneca, Boehringer Ingelheim Pharmaceuticals, Inc., Eisai Inc., GlaxoSmithKline plc., Janssen Pharmaceuticals, Inc., Lexicon Pharmaceuticals, Inc., Ligand Pharmaceuticals, Inc., Eli Lilly and Company, Merck & Co., Inc., Novo Nordisk Inc., Pfizer Inc., Sanofi-Aventis, Takeda Development Center Americas, Inc.. S. Agarwal: None. J.K. Snell-Bergeon: Stock/Shareholder; Self; Abbott. Research Support; Self; Roche Diagnostics Corporation. E. Cengiz: Advisory Panel; Self; Novo Nordisk Inc.. Speaker's Bureau; Self; Novo Nordisk Inc.. Advisory Panel; Self; MannKind Corporation, ADOCIA, Arecor. S. Polsky: Research Support; Self; Dexcom, Inc.. Other Relationship; Self; T1D Exchange. Research Support; Self; National Institute of Diabetes and Digestive and Kidney Diseases. V.N. Shah: None.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db18-15-LB
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
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  • 6
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    Genetic Studies of Leptin Concentrations Implicate Leptin in the Regulation of Early Adiposity
    American Diabetes Association ; 2020
    In:  Diabetes Vol. 69, No. 12 ( 2020-12-01), p. 2806-2818
    Details
    In: Diabetes, American Diabetes Association, Vol. 69, No. 12 ( 2020-12-01), p. 2806-2818
    Abstract: Leptin influences food intake by informing the brain about the status of body fat stores. Rare LEP mutations associated with congenital leptin deficiency cause severe early-onset obesity that can be mitigated by administering leptin. However, the role of genetic regulation of leptin in polygenic obesity remains poorly understood. We performed an exome-based analysis in up to 57,232 individuals of diverse ancestries to identify genetic variants that influence adiposity-adjusted leptin concentrations. We identify five novel variants, including four missense variants, in LEP, ZNF800, KLHL31, and ACTL9, and one intergenic variant near KLF14. The missense variant Val94Met (rs17151919) in LEP was common in individuals of African ancestry only, and its association with lower leptin concentrations was specific to this ancestry (P = 2 × 10−16, n = 3,901). Using in vitro analyses, we show that the Met94 allele decreases leptin secretion. We also show that the Met94 allele is associated with higher BMI in young African-ancestry children but not in adults, suggesting that leptin regulates early adiposity.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db20-0070
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2020
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  • 7
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    Trans Fatty Acid Biomarkers and Incident Type 2 Diabetes: Pooled Analysis of 12 Prospective Cohort Studies in the Fatty Acids and Outcomes Research Consortium (FORCE)
    American Diabetes Association ; 2022
    In:  Diabetes Care Vol. 45, No. 4 ( 2022-04-01), p. 854-863
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 45, No. 4 ( 2022-04-01), p. 854-863
    Abstract: Trans fatty acids (TFAs) have harmful biologic effects that could increase the risk of type 2 diabetes (T2D), but evidence remains uncertain. We aimed to investigate the prospective associations of TFA biomarkers and T2D by conducting an individual participant-level pooled analysis. RESEARCH DESIGN AND METHODS We included data from an international consortium of 12 prospective cohorts and nested case-control studies from six nations. TFA biomarkers were measured in blood collected between 1990 and 2008 from 25,126 participants aged ≥18 years without prevalent diabetes. Each cohort conducted de novo harmonized analyses using a prespecified protocol, and findings were pooled using inverse-variance weighted meta-analysis. Heterogeneity was explored by prespecified between-study and within-study characteristics. RESULTS During a mean follow-up of 13.5 years, 2,843 cases of incident T2D were identified. In multivariable-adjusted pooled analyses, no significant associations with T2D were identified for trans/trans-18:2, relative risk (RR) 1.09 (95% CI 0.94–1.25); cis/trans-18:2, 0.89 (0.73–1.07); and trans/cis-18:2, 0.87 (0.73–1.03). Trans-16:1n-9, total trans-18:1, and total trans-18:2 were inversely associated with T2D (RR 0.81 [95% CI 0.67–0.99], 0.86 [0.75–0.99] , and 0.84 [0.74–0.96], respectively). Findings were not significantly different according to prespecified sources of potential heterogeneity (each P ≥ 0.1). CONCLUSIONS Circulating individual trans-18:2 TFA biomarkers were not associated with risk of T2D, while trans-16:1n-9, total trans-18:1, and total trans-18:2 were inversely associated. Findings may reflect the influence of mixed TFA sources (industrial vs. natural ruminant), a general decline in TFA exposure due to policy changes during this period, or the relatively limited range of TFA levels.
    Type of Medium: Online Resource
    ISSN: 0149-5992
    URL: Article
    DOI: 10.2337/dc21-1756
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2022
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  • 8
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    209-LB: Evidence Thathypothalamic Glucoregulatory Neurons Sense and Respond to Changes of Glycemia in Conscious, Free-Living Mice
    American Diabetes Association ; 2022
    In:  Diabetes Vol. 71, No. Supplement_1 ( 2022-06-01)
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    In: Diabetes, American Diabetes Association, Vol. 71, No. Supplement_1 ( 2022-06-01)
    Abstract: The brain’s capacity to normalize the defended blood glucose level in diabetic animals is now well established. We hypothesized that for this to occur, the brain, like the pancreas, must detect and respond to changes in circulating glucose, but whether and how this occurs remains unknown. To identify specific neuronal subsets that are responsive to changes in glycemia in conscious, free-living mice, we combined continuous arterial glucose monitoring (CGM) with fiber photometry (FP) to measure the calcium activity of neurons located in the hypothalamic ventromedial nucleus that express the peptide, Pacap (VMHPacap neurons) . CGM and FP data from each of six mice were obtained during both a 1-h baseline monitoring period (without access to food) and over a 2-h intervention period in which the blood glucose (BG) level was elevated by either chow or a high-sucrose meal consumption, or by IP glucose injection. Cross-correlation analysis revealed that following a 60-80 s delay, interventions that raise the BG level are reliably associated with significantly reduced VMHPacap neuron activity (p & lt; 0.01) . Interestingly, levels of BG and VMHPacapneuron calcium activity were also significantly correlated under baseline conditions (i.e., in the absence of any intervention) , but unlike what occurs following an intervention, these two variables were positively correlated with a ∼25 min offset, suggestive of an oscillatory pattern. We conclude that after a short delay, physiological stimuli that raise the BG level are coupled to reduced activity of VMHPacap neurons in vivo. In the basal state, levels of these two variables are positivity correlated in a delayed manner suggestive of an oscillatory control mechanism. These findings identify hypothalamic glucoregulatory neurons that are capable of sensing and responding to changes of glycemia in conscious, free-living mice. Disclosure J. D. Deem: None. A. Kumar: None. J. M. Scarlett: None. G. J. Morton: Research Support; Novo Nordisk A/S. M. W. Schwartz: None. D. Tingley: None. A. Bjerregaard: Employee; Novo Nordisk. C. L. Faber: None. T. P. Doan: None. B. N. Phan: None. Z. Nasir: None. B. Wu: None. M. K. Hwang: None. Funding NIDDK:P30 DK035816 K01 DK126793 R01 DK124238 R01 DK83042 NIDA:P30 DA048736; Novo Nordisk Research Agreement:CMS-431104
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db22-209-LB
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2022
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  • 9
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    n-3 Fatty Acid Biomarkers and Incident Type 2 Diabetes: An Individual Participant-Level Pooling Project of 20 Prospective Cohort Studies
    American Diabetes Association ; 2021
    In:  Diabetes Care Vol. 44, No. 5 ( 2021-05-01), p. 1133-1142
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 44, No. 5 ( 2021-05-01), p. 1133-1142
    Abstract: Prospective associations between n-3 fatty acid biomarkers and type 2 diabetes (T2D) risk are not consistent in individual studies. We aimed to summarize the prospective associations of biomarkers of α-linolenic acid (ALA), eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA) with T2D risk through an individual participant-level pooled analysis. RESEARCH DESIGN AND METHODS For our analysis we incorporated data from a global consortium of 20 prospective studies from 14 countries. We included 65,147 participants who had blood measurements of ALA, EPA, DPA, or DHA and were free of diabetes at baseline. De novo harmonized analyses were performed in each cohort following a prespecified protocol, and cohort-specific associations were pooled using inverse variance–weighted meta-analysis. RESULTS A total of 16,693 incident T2D cases were identified during follow-up (median follow-up ranging from 2.5 to 21.2 years). In pooled multivariable analysis, per interquintile range (difference between the 90th and 10th percentiles for each fatty acid), EPA, DPA, DHA, and their sum were associated with lower T2D incidence, with hazard ratios (HRs) and 95% CIs of 0.92 (0.87, 0.96), 0.79 (0.73, 0.85), 0.82 (0.76, 0.89), and 0.81 (0.75, 0.88), respectively (all P & lt; 0.001). ALA was not associated with T2D (HR 0.97 [95% CI 0.92, 1.02]) per interquintile range. Associations were robust across prespecified subgroups as well as in sensitivity analyses. CONCLUSIONS Higher circulating biomarkers of seafood-derived n-3 fatty acids, including EPA, DPA, DHA, and their sum, were associated with lower risk of T2D in a global consortium of prospective studies. The biomarker of plant-derived ALA was not significantly associated with T2D risk.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc20-2426
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2021
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  • 10
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    157-OR: High-Fat–Diet Feeding Disrupts Thermal Responsiveness of AgRP Neurons
    American Diabetes Association ; 2022
    In:  Diabetes Vol. 71, No. Supplement_1 ( 2022-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 71, No. Supplement_1 ( 2022-06-01)
    Abstract: To defend energy homeostasis in the cold requires energy expenditure (to support thermogenesis) and energy intake increase, enabling core temperature to be maintained with no change to body fat stores. When acutely housed at a mild cold (14°C) , mice increase both food intake and heat production rapidly (∼minutes) , and these responses occur in parallel. We hypothesized a role for Agouti-related peptide (AgRP) neurons in this response and find their activity is regulated by thermal sensory input, and they increase activity, measured by Fos induction and fiber photometry, upon cold sensation, and reduce activity as sensed temperatures rise. By inhibiting AgRP neurons during acute cold exposure, we also find this increase in AgRP neuron activity is required for the hyperphagic response to cold. Recent evidence found high-fat diet (HFD) feeding reduced AgRP neuron responsiveness to gastric hormones and standard chow diet presentation, and we hypothesized that their response to thermal input might also be blunted. We find that although 12-week HFD-fed mice exhibit intact thermogenic responses to cold and defend a normal core body temperature, they fail to increase energy intake and consequently experience weight loss not observed in chow-fed controls. This uncoupling of energy intake from energy expenditure is present even after a shorter, 2-week exposure to HFD-feeding, implying a role for diet separate from obesity in the phenotype. Using Agrp-Cre/GFP marker mice, we find acute cold exposure rapidly induces Fos in chow-fed mice, but this response is lacking in HFD-fed mice. This effect correlates with a failure to increase hypothalamic Agrp mRNA even after five days of mild cold exposure. Using photometry to measure AgRP neuron calcium activity, we find activity changes associated with thermal input, both cold and warm, are blunted with HFD feeding. Further testing will determine exactly how the food intake response to cold has become uncoupled from other thermoregulatory responses across the development of obesity. Disclosure J.D.Deem: None. T.P.Doan: None. B.N.Phan: None. K.Ogimoto: None. S.J.W.Hu: None. B.Wu: None. M.W.Schwartz: None. G.J.Morton: Research Support; Novo Nordisk A/S. Funding American Diabetes Association (1-19-PDF-103) ; NIDDK (K01 DK126793) , NIDDK (DK089056) , NIDDK (DK124238) , NIDDK (DK035816) , NIDA (P30 DA048736) , NIDDK (DK035816) , NIDDK (DK17047)
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db22-157-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2022
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