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  • 1
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    Online Resource
    81-OR: High Throughput Proteomics Identifies Neurofilament Light Chain (NFL) as a Novel Blood Biomarker for Detection of Diabetic Sensorimotor Polyneuropathy
    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: Background: The neurofilament light chain (NFL) is a polypeptide abundant in neuronal axons, reflecting ongoing neuroaxonal degeneration when detected in the blood. However, no previous study has explored NFL as a potential biomarker for diabetic sensorimotor polyneuropathy (DSPN) , a neurodegenerative disease of the peripheral nervous system commonly found in individuals with diabetes. We hypothesized that higher serum NFL levels are associated with DSPN. Methods: We used data from the German Diabetes Study, a prospective observational study that includes adults with recent-onset diabetes ( & lt;1 year) . DSPN was assessed using Toronto consensus criteria. Serum levels of NFL were measured using proximity extension assay, and Poisson regression was used to estimate associations between serum NFL and prevalent DSPN. Results: From a total of 423 participants, 66 (16%) had DSPN. Serum NFL was inversely correlated with age, eGFR and nerve conduction velocities in motor and sensory nerves (all P Spearman & lt;0.0001) . After adjustment for age, sex, waist circumference, height, HbA1c, diabetes duration, diabetes type, cholesterol, eGFR, hypertension, cardiovascular diseases, use of lipid-lowering drugs, and NSAIDs, higher serum levels of NFL were associated with prevalent DSPN (RR (95% CI) 1.92 (1.50, 2.45) (P & lt; 0.0001) . Conclusion: NFL might be useful for detecting DSPN in recent-onset diabetes, but validation in other studies will be required. Considering the absence of FDA-approved biomarkers for DSPN, NFL might be a promising biomarker that could improve the management of DSPN. Disclosure H. Maalmi: None. A. Strom: None. S.M. Hauck: None. G.J. Bönhof: None. W. Rathmann: Consultant; IQVIA Inc. Speaker's Bureau; Boehringer Ingelheim International GmbH, Novo Nordisk. S. Trenkamp: None. V. Burkart: None. J.M. Szendroedi: Consultant; Boehringer Ingelheim International GmbH. D. Ziegler: None. M. Roden: Advisory Panel; Eli Lilly and Company. Research Support; Boehringer Ingelheim International GmbH, Nutricia. Speaker's Bureau; Novo Nordisk. C. Herder: Research Support; Sanofi. Funding DZD (FKZ82DZD02D2G)
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db22-81-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2022
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  • 2
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    1300-P: Visceral Adipose Tissue Volume Is Increased in Severe Insulin Resistant Diabetes
    American Diabetes Association ; 2024
    In:  Diabetes Vol. 73, No. Supplement_1 ( 2024-06-14)
    Details
    In: Diabetes, American Diabetes Association, Vol. 73, No. Supplement_1 ( 2024-06-14)
    Abstract: Introduction & Objective: The severe insulin resistant diabetes (SIRD) endotype associates with markedly higher risk of metabolic dysfunction associated steatotic liver disease (MASLD). However, it is not known if ectopic lipid deposition is also higher in skeletal muscle or adipose tissue compartments than in other endotypes. Methods: Participants (n=697, known diabetes duration & lt;1 y) of the prospective German Diabetes Study (GDS) underwent 1H magnetic resonance spectroscopy for quantifying intramyocellular lipids (IMCL) in tibialis anterior muscle, intrahepatic lipids (IHL), visceral (VAT) and subcutaneous adipose tissue (SAT) volumes. The validated clustering algorithm used age, sex, BMI, HOMA-IR, HOMA-B, islet-directed autoantibodies. Results: As expected, SIRD (n=40) had the highest IHL (11±5%) compared to mean IHL values of 2-6% in moderate obesity-related (MOD, n=215), moderate age-related (MARD, n=237) and severe autoimmune diabetes clusters (SAID, n=193; all p & lt;0.01). Interestingly, SIRD presented with higher VAT than MOD, MARD and SAID (6089±2705 vs 3260±2310, 3056±1963, 1524±1401 cm3) even after adjustment for BMI (all p & lt;0.05). Also, SAT was higher in SIRD than MARD (27879±6777 vs 17127±6218 cm3, p & lt;0.05), while differences to other subtypes lost statistical significance upon correction for BMI. There were no differences in IMCL between subtypes. Overall, VAT correlated with cardiovascular risk (Framingham, r=0.661, p & lt;0.05), whole-body insulin sensitivity derived from hyperinsulinemic euglycemic clamp (r=-0.537, p & lt;0.05) and with beta cell function during intravenous glucose tolerance test (r=0.379, p & lt;0.05). Within SIRD, VAT was further associated with fasting glycemia (r=0.121, p=0.05) and fasting insulin resistance (HOMA-IR; r=0.372, p & lt;0.05). Conclusion: The increases in IHL and VAT underline their key role in the pathophysiology and progression of severely insulin resistant diabetes and shall help to refine subtyping approaches for precision diabetology. Disclosure O.P. Zaharia: None. Y. Kupriyanova: None. P. Bobrov: None. M. Schön: None. C. Möser: None. N. Trinks: None. D.M. Mendez Cardenas: None. S. Trenkamp: None. K. Bódis: None. V. Schrauwen-Hinderling: None. R. Wagner: Speaker's Bureau; Sanofi. Advisory Panel; Lilly Diabetes. Speaker's Bureau; Boehringer-Ingelheim, Novo Nordisk. M. Roden: Advisory Panel; Eli Lilly and Company. Research Support; Boehringer-Ingelheim. Advisory Panel; Novo Nordisk. Research Support; Novo Nordisk. Advisory Panel; TARGET PharmaSolutions, Inc. Speaker's Bureau; AstraZeneca. Funding EFSD Rising Star Award
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db24-1300-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2024
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  • 3
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    293-OR: Improvement of Tissue-Specific Insulin Sensitivity after Bariatric Surgery Does Not Restore Hepatic OXPHOS Capacity
    American Diabetes Association ; 2024
    In:  Diabetes Vol. 73, No. Supplement_1 ( 2024-06-14)
    Details
    In: Diabetes, American Diabetes Association, Vol. 73, No. Supplement_1 ( 2024-06-14)
    Abstract: Common insulin resistance relates to positive energy balance and is central to obesity, type 2 diabetes and metabolic dysfunction-associated steatotic liver disease (MASLD). In early MASLD, the liver adapts to increased energy supply by upregulating its oxidative phosphorylation (OXPHOS) capacity (mitochondrial plasticity), which is lost during MASLD progression and in type 2 diabetes. This study examined whether improvements in insulin sensitivity after bariatric surgery restore hepatic mitochondrial plasticity and thereby ameliorate liver histology. Persons with insulin resistance and obesity (n=16, BMI 52±8 kg/m2; HbA1c 5.5±0.1%) underwent bariatric and follow-up surgeries, at which liver biopsies were taken. MASLD was assessed histologically. Hepatic maximal ADP-stimulated respiration, reflecting OXPHOS capacity, was measured by high-resolution respirometry, tissue-specific insulin sensitivity by hyperinsulinemic-euglycemic clamps with 2H2-glucose. Mean body weight loss (-48.5 kg over 0.5-5 years) increased whole-body (stimulated glucose disposal) as well as hepatic (suppressed endogenous glucose production) insulin sensitivity by 57 and 32% (both p & lt;0.05), respectively. Fasting adipose tissue insulin resistance (Adipo-IR) decreased by 61% (p=0.005). Steatosis grade decreased in all participants, whereas lobular inflammation and ballooning did not uniformly change after surgery. Hepatic mitochondrial DNA (mtDNA) content slightly rose (p=0.02), whereas OXPHOS capacity remained unchanged for TCA cycle- and β-oxidation-linked respiration upon normalization for both tissue wet weight and mtDNA. In conclusion, bariatric surgery led to robust improvements in whole-body, hepatic and adipose tissue insulin sensitivity as well as hepatic steatosis. However, the failure to restore hepatic mitochondrial plasticity and to reverse inflammation indicates the need for novel mitochondria-targeted concepts for MASLD treatment. Disclosure S. Kahl: None. J. Puetzer-Furmanczak: None. N. Trinks: None. B. Dewidar: None. K. Pafili: None. S. Trenkamp: None. I. Esposito: None. M. Schlensak: None. F.A. Granderath: None. M. Roden: Advisory Panel; Eli Lilly and Company. Research Support; Boehringer-Ingelheim. Advisory Panel; Novo Nordisk. Research Support; Novo Nordisk. Advisory Panel; TARGET PharmaSolutions, Inc. Speaker's Bureau; AstraZeneca. Funding German Federal Ministry of Health (BMG); Ministry of Culture and Science of the State North Rhine-Westphalia (MKW NRW) to DDZGerman Federal Ministry of Education and Research (BMBF) to German Center for Diabetes Research (DZD e. V.). HORIZON-HLTH-2022-STAYHLTH-02-01: Panel A to the INTERCEPT-T2D consortium EUREKA Eurostars-2 (E!-113230-DIA-PEP)German Science Foundation (DFG; SFB/CRC1116, RTG/GRK 2576) Schmutzler-Stiftung "Profilbildung 2020"
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db24-293-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2024
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  • 4
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    302-OR: How Menstrual Cycle Impacts Brain Insulin Action—Results from Young Women
    American Diabetes Association ; 2023
    In:  Diabetes Vol. 72, No. Supplement_1 ( 2023-06-20)
    Details
    In: Diabetes, American Diabetes Association, Vol. 72, No. Supplement_1 ( 2023-06-20)
    Abstract: The human brain is an insulin-sensitive organ that modulates whole-body glucose metabolism and adiposity. In case of brain insulin resistance, this regulation is disturbed. In the periphery, insulin sensitivity varies along the menstrual cycle, while the effects on brain insulin action are still unknown. We here investigated the impact of menstrual cycle on brain insulin sensitivity of the human hypothalamus and on brain-derived modulation of peripheral metabolism. In 26 naturally cycling women (age 19-29 years, BMI 18-24 kg/m2), brain insulin action was assessed in both the follicular and the luteal phase using nasal application of 160 U insulin. In fifteen women, we assessed hypothalamic insulin responsiveness by functional MRI combined with nasal insulin. In eleven women, brain-derived modulation of peripheral insulin sensitivity was studied by hyperinsulinemic euglycemic clamps combined with insulin vs placebo spray. Only in the follicular phase, nasal insulin significantly decreased hypothalamic blood flow (p=0.02), indicating proper brain insulin action. In the luteal phase, insulin induced no such effect (p=0.6). During hyperinsulinemic euglycemic clamps in the follicular phase, more glucose had to be infused after insulin compared to placebo spray. This difference remained significant after adjustment for circulating glucose and insulin (p & lt;0.0001), which was not the case in the luteal phase (p=0.1). High estradiol/progesterone ratio, as present during the follicular phase, was linked to a stronger effect of insulin spray on glucose infusion rates than placebo. Brain insulin sensitivity is a regulated process that can rapidly adapt to changing physiologic requirements, as through the menstrual cycle. In the luteal phase, we detected hypothalamic insulin resistance, which likely contributed to the lacking modulation of peripheral insulin sensitivity through brain insulin delivery. Thus, brain insulin resistance could contribute to whole-body insulin resistance in the luteal phase. Disclosure J.Hummel: None. M.Roden: Advisory Panel; Eli Lilly and Company, Consultant; TARGET PharmaSolutions, Inc., Research Support; Boehringer-Ingelheim, Novo Nordisk, Novartis, Sanofi. H.Häring: None. A.Fritsche: Advisory Panel; Novo Nordisk, Lilly, Sanofi, Boehringer-Ingelheim, Speaker's Bureau; AstraZeneca, SYNLAB Holding Deutschland GmbH. A.Peter: None. R.Wagner: Advisory Panel; Daiichi Sankyo, Speaker's Bureau; Novo Nordisk, Sanofi. S.Kullmann: None. M.Heni: Advisory Panel; Boehringer-Ingelheim, Sanofi, Research Support; Boehringer Ingelheim Inc., Speaker's Bureau; Lilly, Bayer Inc., Sanofi, Boehringer-Ingelheim, Novo Nordisk, Amryt Pharma Plc. C.Benkendorff: None. L.Fritsche: None. K.Prystupa: Other Relationship; Berlin-Chemie AG. A.Vosseler: None. S.Gancheva: Consultant; Novo Nordisk, Bayer Inc. S.Trenkamp: None. A.L.Birkenfeld: None. H.Preissl: None. Funding German Federal Ministry of Education and Research
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db23-302-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2023
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  • 5
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    1573-P: Association of Thyroid Hormone Levels with NAFLD in Recent-Onset Diabetes
    American Diabetes Association ; 2023
    In:  Diabetes Vol. 72, No. Supplement_1 ( 2023-06-20)
    Details
    In: Diabetes, American Diabetes Association, Vol. 72, No. Supplement_1 ( 2023-06-20)
    Abstract: Nonalcoholic fatty liver disease (NAFLD) is a growing health concern associated with obesity and type 2 diabetes (T2D). Thyroid hormones are important regulators of lipid homeostasis. Indeed, people with hypothyroidism are at greater risk for NAFLD and it has been suggested that humans with T2D are more likely to develop hypothyroidism. However, little is known about the relationship of thyroid function with NAFLD in type 1 diabetes (T1D) and T2D. We hypothesized that (i) low free thyroxin (fT4) and high thyroid-stimulating hormone (TSH) levels are associated with increased hepatocellular lipid content (HCL) and (ii) that fT4 and TSH can identify persons at high-risk for hepatic steatosis in people with recent-onset diabetes. We examined people with T1D (n=358) or T2D (n=596) and 175 healthy participants of the German Diabetes Study (GDS). First, validation of the fatty liver index (FLI) against quantification of HCL by 1H-magnetic resonance spectroscopy revealed a close correlation (ß=0.715, p & lt;0.001; n=446). Second, FLI negatively correlated with fT4 in males (ß=−0.139, p & lt;0.01), but not in females with T2D (ß=−0.086, p=0.26). Likewise, TSH associated positively with FLI in males (ß=0.116, p & lt;0.05), but not in females with T2D (ß=−0.057, p=0.45). TSH and FLI were differently associated between males and females before (p & lt;0.05), but not after (p=0.82) adjustment for BMI. Finally, fT4 had a low diagnostic precision for steatosis (by FLI) as derived from the respective area under the receiver operating curve (0.57, 95% CI [0.53;0.62]; p & lt;0.001) in T2D and was not significant in other groups. TSH had no diagnostic precision for steatosis in any groups. In conclusion, FLI can be used as a surrogate measure of HCL in recent-onset diabetes. The correlation of FLI with lower thyroid function in male T2D suggests a sex-specific interaction between thyroid and liver lipid metabolism, which is mainly driven by body mass. Both, fT4 and TSH offer no relevant efficacy to detect steatosis at least in recent-onset diabetes. Disclosure N. Saatmann: None. M. Schön: None. O.P. Zaharia: None. M. Huttasch: None. K. Strassburger: None. S. Trenkamp: None. Y. Kupriyanova: None. V. Schrauwen-Hinderling: None. S. Kahl: None. V. Burkart: None. R. Wagner: Speaker's Bureau; Novo Nordisk, Sanofi. Advisory Panel; Daiichi Sankyo. M. Roden: Advisory Panel; Eli Lilly and Company. Research Support; Boehringer-Ingelheim, Novo Nordisk, Novartis. Consultant; TARGET PharmaSolutions, Inc. Research Support; Sanofi.
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db23-1573-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2023
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