{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T04:22:10Z","timestamp":1770265330059,"version":"3.49.0"},"reference-count":49,"publisher":"American Diabetes Association","issue":"2","content-domain":{"domain":["diabetesjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,2,1]]},"abstract":"<jats:p>OBJECTIVE\u2014To determine whether first-degree relatives of individuals with type 2 diabetes, who are at high risk of subsequently developing hyperglycemia, manifest alterations in \u03b2-cell function including an alteration in the co-release of insulin and amylin.<\/jats:p>\n               <jats:p>RESEARCH DESIGN AND METHODS\u2014In 30 first-degree relatives and 24 matched subjects with no family history of diabetes, \u03b2-cell function was measured as the intravenous glucose-induced acute insulin response (AIRg) and acute amylin response (AARg). The insulin sensitivity index (SI) was quantified and used to account for the role of insulin sensitivity to modulate \u03b2-cell function (SI \u00d7 \u03b2-cell function).<\/jats:p>\n               <jats:p>RESULTS\u2014Fasting plasma glucose (5.3 \u00b1 0.1 vs. 5.1 \u00b1 0.1 mmol\/l; means \u00b1 SEM), immunoreactive insulin (IRI) (68 \u00b1 7 vs. 57 \u00b1 6 pmol\/l) and amylin-like immunoreactivity (ALI) (5.5 \u00b1 0.6 vs. 4.7 \u00b1 0.7 pmol\/l) were similar in relatives and control subjects, respectively. Relatives were insulin resistant compared with control subjects (SI: 4.86 \u00b1 0.63 vs. 7.20 \u00b1 0.78 \u00d7 10\u22125 min\u22121 \u00b7 pmol\u22121 \u00b7 l\u22121, P = 0.01), but their AIRg (392 \u00b1 59 vs. 386 \u00b1 50 pmol\/l) and AARg (5.9 \u00b1 0.9 vs. 6.1 \u00b1 0.8 pmol\/l) did not differ. When \u03b2-cell function was determined relative to insulin sensitivity, in the first-degree relatives, both AIRg (SI \u00d7 AIRg: 1.60 \u00b1 0.23 vs. 2.44 \u00b1 0.31 \u00d7 10\u22122 min\u22121, P &amp;lt; 0.05) and AARg (SI \u00d7 AARg: 2.39 \u00b1 0.35 vs. 4.06 \u00b1 0.56 \u00d7 10\u22124 min\u22121, P &amp;lt; 0.05) were reduced. The molar proportion of ALI to IRI was not altered in high-risk subjects (1.75 \u00b1 0.16 vs. 1.71 \u00b1 0.15%).<\/jats:p>\n               <jats:p>CONCLUSIONS\u2014First-degree relatives of subjects with type 2 diabetes have diminished \u03b2-cell function at a time when they are not hyperglycemic, and this reduction affects insulin and amylin responses proportionally. Thus, an altered amylin-to-insulin ratio is not likely to identify individuals at high risk of developing type 2 diabetes.<\/jats:p>","DOI":"10.2337\/diacare.25.2.292","type":"journal-article","created":{"date-parts":[[2007,3,5]],"date-time":"2007-03-05T22:51:27Z","timestamp":1173135087000},"page":"292-297","update-policy":"https:\/\/doi.org\/10.2337\/ada-journal-policies","source":"Crossref","is-referenced-by-count":36,"title":["Insulin and Amylin Release Are Both Diminished in First-Degree Relatives of Subjects With Type 2 Diabetes"],"prefix":"10.2337","volume":"25","author":[{"given":"Negar G.","family":"Knowles","sequence":"first","affiliation":[{"name":"From the Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System, and the University of Washington, Seattle, Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Melinda A.","family":"Landchild","sequence":"additional","affiliation":[{"name":"From the Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System, and the University of Washington, Seattle, Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wilfred Y.","family":"Fujimoto","sequence":"additional","affiliation":[{"name":"From the Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System, and the University of Washington, Seattle, Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Steven E.","family":"Kahn","sequence":"additional","affiliation":[{"name":"From the Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, VA Puget Sound Health Care System, and the University of Washington, Seattle, Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1167","reference":[{"key":"2022031216064760700_R1","unstructured":"Kahn SE, Porte D Jr: Pathophysiology of type II diabetes mellitus. In Diabetes Mellitus. Porte D Jr, Sherwin RS, Eds. Stamford, CT, Appleton & Lange, 1996, p. 487\u2013512"},{"key":"2022031216064760700_R2","doi-asserted-by":"crossref","unstructured":"Porte D Jr: \u03b2-Cells in type II diabetes mellitus. Diabetes\u200840: 166\u2013180, 1991","DOI":"10.2337\/diab.40.2.166"},{"key":"2022031216064760700_R3","doi-asserted-by":"crossref","unstructured":"Sanke T, Hanabusa T, Nakano Y, Oki C, Okai K, Nishimura S, Kondo M, Nanjo K: Plasma islet amyloid polypeptide (amylin) levels and their responses to oral glucose in type 2 (non-insulin-dependent) diabetic patients. Diabetologia\u200834:129\u2013132, 1991","DOI":"10.1007\/BF00500385"},{"key":"2022031216064760700_R4","doi-asserted-by":"crossref","unstructured":"Enoki S, Mitsukawa T, Takemura J, Nakazato M, Aburaya J, Toshimori H, Matsukara S: Plasma islet amyloid polypeptide levels in obesity, impaired glucose tolerance and non-insulin-dependent diabetes mellitus. Diabetes Res Clin Pract\u200815:97\u2013102, 1992","DOI":"10.1016\/0168-8227(92)90074-2"},{"key":"2022031216064760700_R5","doi-asserted-by":"crossref","unstructured":"Kahn SE, Verchere CB, Andrikopoulos S, Asberry PJ, Leonetti DL, Wahl PW, Boyko EJ, Schwartz RS, Newell-Morris L, Fujimoto WY: Reduced amylin release is a characteristic of impaired glucose tolerance and type 2 diabetes in Japanese Americans. Diabetes\u200847:640\u2013645, 1998","DOI":"10.2337\/diabetes.47.4.640"},{"key":"2022031216064760700_R6","doi-asserted-by":"crossref","unstructured":"Haffner S, Stern M, Hazuda H, Mitchell B, Patterson J: Increased insulin concentrations in nondiabetic offspring of diabetic parents. N Engl J Med\u2008319:1297\u20131301, 1988","DOI":"10.1056\/NEJM198811173192001"},{"key":"2022031216064760700_R7","doi-asserted-by":"crossref","unstructured":"Lillioja S, Mott DM, Howard BV, Bennett PH, Yki-Jarvinen H, Freymond D, Nyomba BL, Zurlo F, Swinburn B, Bogardus C: Impaired glucose tolerance as a disorder of insulin action: longitudinal and cross-sectional studies in Pima Indians. N Engl J Med\u2008318:1217\u20131225, 1988","DOI":"10.1056\/NEJM198805123181901"},{"key":"2022031216064760700_R8","doi-asserted-by":"crossref","unstructured":"Warram JH, Martin BC, Krolewski AS, Soeldner JS, Kahn CR: Slow glucose removal rate and hyperinsulinemia precede the development of type II diabetes in the offspring of diabetic parents. Ann Intern Med\u2008113:909\u2013915, 1990","DOI":"10.7326\/0003-4819-113-12-909"},{"key":"2022031216064760700_R9","doi-asserted-by":"crossref","unstructured":"Martin BL, Warram JH, Krolewski AS, Bergman RN, Soeldner JS, Kahn CR: Role of glucose and insulin resistance in development of type 2 diabetes mellitus: results of a 25-year follow-up study. Lancet\u2008340:925\u2013929, 1992","DOI":"10.1016\/0140-6736(92)92814-V"},{"key":"2022031216064760700_R10","doi-asserted-by":"crossref","unstructured":"Eriksson J, Franssila Kallunki A, Ekstrand A, Saloranta C, Widen E, Schalin C, Groop L: Early metabolic defects in persons at increased risk for non-insulin-dependent diabetes mellitus. N Engl J Med\u2008321:337\u2013343, 1989","DOI":"10.1056\/NEJM198908103210601"},{"key":"2022031216064760700_R11","doi-asserted-by":"crossref","unstructured":"Lillioja S, Mott DM, Spraul M, Ferraro R, Foley JE, Ravussin E, Knowler WC, Bennett PH, Bogardus C: Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus: prospective studies of Pima Indians. N Engl J Med\u2008329:1988\u20131992, 1993","DOI":"10.1056\/NEJM199312303292703"},{"key":"2022031216064760700_R12","doi-asserted-by":"crossref","unstructured":"Bergman RN, Phillips LS, Cobelli C: Physiologic evaluation of factors controlling glucose tolerance in man: measurement of insulin sensitivity and \u03b2-cell glucose sensitivity from the response to intravenous glucose. J Clin Invest\u200868:1456\u20131467, 1981","DOI":"10.1172\/JCI110398"},{"key":"2022031216064760700_R13","doi-asserted-by":"crossref","unstructured":"Kahn SE, Prigeon RL, McCulloch DK, Boyko EJ, Bergman RN, Schwartz MW, Neifing JL, Ward WK, Beard JC, Palmer JP, Porte D Jr: Quantification of the relationship between insulin sensitivity and B-cell function in human subjects: evidence for a hyperbolic function. Diabetes\u200842:1663\u20131672, 1993","DOI":"10.2337\/diabetes.42.11.1663"},{"key":"2022031216064760700_R14","doi-asserted-by":"crossref","unstructured":"Ryan EA, Imes S, Liu D, McManus R, Finegood DT, Polonsky KS, Sturis J: Defects in insulin secretion and action in women with a history of gestational diabetes. Diabetes\u200844:506\u2013512, 1995","DOI":"10.2337\/diabetes.44.5.506"},{"key":"2022031216064760700_R15","doi-asserted-by":"crossref","unstructured":"Larsson H, Ahren B: Failure to adequately adapt reduced insulin sensitivity with increased insulin secretion in women with impaired glucose tolerance. Diabetologia\u200839:1099\u20131107, 1996","DOI":"10.1007\/BF00400660"},{"key":"2022031216064760700_R16","doi-asserted-by":"crossref","unstructured":"Cavaghan MK, Ehrmann DA, Byrne MM, Polonsky KS: Treatment with the oral antidiabetic agent troglitazone improves beta cell responses to glucose in subjects with impaired glucose tolerance. J Clin Invest\u2008100:530\u2013537, 1997","DOI":"10.1172\/JCI119562"},{"key":"2022031216064760700_R17","doi-asserted-by":"crossref","unstructured":"Weyer C, Bogardus C, Mott DM, Pratley RE: The natural history of insulin secretory dysfunction and insulin resistance in the pathogenesis of type 2 diabetes mellitus. J Clin Invest\u2008104:787\u2013794, 1999","DOI":"10.1172\/JCI7231"},{"key":"2022031216064760700_R18","doi-asserted-by":"crossref","unstructured":"Buchanan TA, Xiang AH, Kjos SL, Trigo E, Lee WP, Peters RK: Antepartum predictors of the development of type 2 diabetes in Latino women 11\u201326 months after pregnancies complicated by gestational diabetes. Diabetes\u200848:2430\u20132436, 1999","DOI":"10.2337\/diabetes.48.12.2430"},{"key":"2022031216064760700_R19","doi-asserted-by":"crossref","unstructured":"Butler PC, Chou J, Carter WB, Wang Y-N, Bu B-H, Chang D, Chang J-K, Rizza RA: Effects of meal ingestion on plasma amylin concentration in NIDDM and nondiabetic humans. Diabetes\u200839:752\u2013756, 1990","DOI":"10.2337\/diabetes.39.6.752"},{"key":"2022031216064760700_R20","doi-asserted-by":"crossref","unstructured":"Dechenes CJ, Verchere CB, Andrikopoulos S, Kahn SE: Human aging is associated with parallel reductions in insulin and amylin release. Am J Physiol\u2008275:E785\u2013E791, 1998","DOI":"10.1152\/ajpendo.1998.275.5.E785"},{"key":"2022031216064760700_R21","doi-asserted-by":"crossref","unstructured":"Westermark P, Wernstedt C, Wilander E, Hayden DW, O\u2019Brien TD, Johnson KH: Amyloid fibrils in human insulinoma and islets of Langerhans of the diabetic cat are derived from a neuropeptide-like protein also present in normal islets. Proc Natl Acad Sci U S A\u200884:3881\u20133885, 1987","DOI":"10.1073\/pnas.84.11.3881"},{"key":"2022031216064760700_R22","doi-asserted-by":"crossref","unstructured":"Cooper GJS, Willis AC, Clark A, Turner RC, Sim RB, Reid KBM: Purification and characterization of a peptide from amyloid-rich pancreases of type 2 diabetic patients. Proc Natl Acad Sci U S A\u200884:8628\u20138632, 1987","DOI":"10.1073\/pnas.84.23.8628"},{"key":"2022031216064760700_R23","doi-asserted-by":"crossref","unstructured":"Clark A, Saad MF, Nezzer T, Uren C, Knowler WC, Bennett PH, Turner RC: Islet amyloid polypeptide in diabetic and non-diabetic Pima Indians. Diabetologia\u200833:285\u2013289, 1990","DOI":"10.1007\/BF00403322"},{"key":"2022031216064760700_R24","doi-asserted-by":"crossref","unstructured":"Porte D Jr, Kahn SE: Hyperproinsulinemia and amyloid in NIDDM: clues to etiology of islet \u03b2-cell dysfunction? Diabetes\u200838:1333\u20131336, 1989","DOI":"10.2337\/diabetes.38.11.1333"},{"key":"2022031216064760700_R25","doi-asserted-by":"crossref","unstructured":"Kautzky-Willer A, Thomaseth K, Pacini G, Clodi M, Ludvik B, Streli C, Waldhausl W, Prager R: Role of islet amyloid polypeptide secretion in insulin-resistant humans. Diabetologia\u200837:188\u2013194, 1994","DOI":"10.1007\/s001250050092"},{"key":"2022031216064760700_R26","doi-asserted-by":"crossref","unstructured":"Kautzky-Willer A, Thomaseth K, Ludvik B, Nowotny P, Rabensteiner D, Waldhausl W, Pacini G, Prager R: Elevated islet amyloid pancreatic polypeptide and proinsulin in lean gestational diabetes. Diabetes\u200846:607\u2013614, 1997","DOI":"10.2337\/diabetes.46.4.607"},{"key":"2022031216064760700_R27","doi-asserted-by":"crossref","unstructured":"Prigeon RL, Kahn SE, Porte D Jr: Reliability of error estimates from the minimal model: implications for measurements in physiological studies. Am J Physiol\u2008266:E279\u2013E286, 1994","DOI":"10.1152\/ajpendo.1994.266.2.E279"},{"key":"2022031216064760700_R28","doi-asserted-by":"crossref","unstructured":"Bergman RN, Ider YZ, Bowden CR, Cobelli C: Quantitative estimation of insulin sensitivity. Am J Physiol\u2008236:E667\u2013E677, 1979","DOI":"10.1152\/ajpendo.1979.236.6.E667"},{"key":"2022031216064760700_R29","doi-asserted-by":"crossref","unstructured":"Percy AJ, Trainor DA, Rittenhouse J, Phelps J, Koda JE: Development of sensitive immunoassays to detect amylin and amylin-like peptides in unextracted plasma. Clin Chem\u200842:576\u2013585, 1996","DOI":"10.1093\/clinchem\/42.4.576"},{"key":"2022031216064760700_R30","unstructured":"Rittenhouse J, Chait BT, Bierle JR, Janes SM, Park DR, Phelps JL, Fineman MS, Qin J, Koda JE: Heterogeneity of naturally-occurring human amylin due to glycosylation. Diabetes\u200845 (Suppl. 2):235A, 1996"},{"key":"2022031216064760700_R31","doi-asserted-by":"crossref","unstructured":"Kahn SE, Klaff LJ, Schwartz MW, Beard JC, Bergman RN, Taborsky GJ Jr, Porte D Jr: Treatment with a somatostatin analog decreases pancreatic B-cell and whole body sensitivity to glucose. J Clin Endocrinol Metab\u200871:994\u20131002, 1990","DOI":"10.1210\/jcem-71-4-994"},{"key":"2022031216064760700_R32","doi-asserted-by":"crossref","unstructured":"Clausen JO, Borch-Johnsen K, Ibsen H, Bergman RN, Hougaard P, Winther K, Pedersen O: Insulin sensitivity index, acute insulin response, and glucose effectiveness in a population-based sample of 380 young healthy Caucasians: analysis of the impact of gender, body fat, physical fitness, and life-style factors. J Clin Invest\u200898:1195\u20131209, 1996","DOI":"10.1172\/JCI118903"},{"key":"2022031216064760700_R33","doi-asserted-by":"crossref","unstructured":"Elbein SC, Hasstedt SJ, Wegner K, Kahn SE: Heritability of pancreatic beta-cell function among nondiabetic members of Caucasian familial type 2 diabetic kindreds. J Clin Endocrinol Metab\u200884:1398\u20131403, 1999","DOI":"10.1210\/jc.84.4.1398"},{"key":"2022031216064760700_R34","doi-asserted-by":"crossref","unstructured":"Kahn SE, Prigeon RL, McCulloch DK, Boyko EJ, Bergman RN, Schwartz MW, Neifing JL, Ward WK, Beard JC, Palmer J, Porte D Jr: The contribution of insulin dependent and insulin independent glucose uptake to intravenous glucose tolerance in healthy human subjects. Diabetes\u200843:587\u2013592, 1994","DOI":"10.2337\/diab.43.4.587"},{"key":"2022031216064760700_R35","doi-asserted-by":"crossref","unstructured":"Best JD, Kahn SE, Ader M, Watanabe RM, Ni TC, Bergman RN: Role of glucose effectiveness in the determination of glucose tolerance. Diabetes Care\u200819:1018\u20131030, 1996","DOI":"10.2337\/diacare.19.9.1018"},{"key":"2022031216064760700_R36","doi-asserted-by":"crossref","unstructured":"Kahn SE, D\u2019Alessio DA, Schwartz MW, Fujimoto WY, Ensinck JW, Taborsky GJ Jr, Porte D Jr: Evidence of cosecretion of islet amyloid polypeptide and insulin by \u03b2-cells. Diabetes\u200839:634\u2013638, 1990","DOI":"10.2337\/diab.39.5.634"},{"key":"2022031216064760700_R37","unstructured":"Landchild MJ, Knowles NG, Yao Q, Walden CE, Retzlaff BM, Knopp RH, Kahn SE: Increased \u03b2-cell secretory demand is not the simple explanation for inefficient proinsulin processing and islet amyloid formation in type 2 diabetes. J Invest Med\u200848:21A, 2000"},{"key":"2022031216064760700_R38","doi-asserted-by":"crossref","unstructured":"Lukinius A, Wilander E, Westermark GT, Engstrom U, Westermark P: Co-localization of islet amyloid polypeptide and insulin in the B cell secretory granules of the human pancreatic islets. Diabetologia\u200832:240\u2013244, 1989","DOI":"10.1007\/BF00285291"},{"key":"2022031216064760700_R39","doi-asserted-by":"crossref","unstructured":"O\u2019Brien TD, Westermark P, Johnson KH: Islet amyloid polypeptide and insulin secretion from isolated perfused pancreas of fed, fasted, glucose-treated, and dexamethasone-treated rats. Diabetes\u200840:1701\u20131706, 1991","DOI":"10.2337\/diabetes.40.12.1701"},{"key":"2022031216064760700_R40","doi-asserted-by":"crossref","unstructured":"Gedulin B, Cooper GJS, Young AA: Amylin secretion from the perfused pancreas: dissociation from insulin and abnormal elevation in insulin-resistant diabetic rats. Biochem Biophys Res Commun\u2008180:782\u2013789, 1991","DOI":"10.1016\/S0006-291X(05)81133-7"},{"key":"2022031216064760700_R41","doi-asserted-by":"crossref","unstructured":"Kahn SE, Verchere CB, D\u2019Alessio DA, Cook DL, Fujimoto WY: Evidence for selective release of rodent islet amyloid polypeptide through the constitutive secretory pathway. Diabetologia\u200836:570\u2013573, 1993","DOI":"10.1007\/BF02743276"},{"key":"2022031216064760700_R42","doi-asserted-by":"crossref","unstructured":"DeFronzo RA: Glucose intolerance of aging: evidence for tissue insensitivity to insulin. Diabetes\u200828:1095\u20131101, 1979","DOI":"10.2337\/diab.28.12.1095"},{"key":"2022031216064760700_R43","doi-asserted-by":"crossref","unstructured":"Chen M, Bergman RN, Pacini G, Porte D Jr: Pathogenesis of age-related glucose intolerance in man: insulin resistance and decreased \u03b2-cell function. J Clin Endocrinol Metab\u200860:13\u201320, 1985","DOI":"10.1210\/jcem-60-1-13"},{"key":"2022031216064760700_R44","doi-asserted-by":"crossref","unstructured":"Mako ME, Starr JI, Rubenstein AH: Circulating proinsulin in patients with maturity-onset diabetes. Am J Med\u200863:865\u2013869, 1977","DOI":"10.1016\/0002-9343(77)90538-1"},{"key":"2022031216064760700_R45","doi-asserted-by":"crossref","unstructured":"Temple RC, Carrington CA, Luzio SD, Owens DR, Schneider AE, Sobey WJ, Hales CN: Insulin deficiency in non-insulin-dependent diabetes. Lancet\u2008i:293\u2013295, 1989","DOI":"10.1016\/S0140-6736(89)91306-8"},{"key":"2022031216064760700_R46","doi-asserted-by":"crossref","unstructured":"Saad MF, Kahn SE, Nelson RG, Pettitt DJ, Knowler WC, Schwartz MW, Kowalyk S, Bennett PH, Porte D Jr: Disproportionately elevated proinsulin in Pima Indians with noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab\u200870:1247\u20131253, 1990","DOI":"10.1210\/jcem-70-5-1247"},{"key":"2022031216064760700_R47","doi-asserted-by":"crossref","unstructured":"Kahn SE, Halban PA: Release of incompletely processed proinsulin is the cause of the disproportionate proinsulinemia of NIDDM. Diabetes\u200846:1725\u20131732, 1997","DOI":"10.2337\/diabetes.46.11.1725"},{"key":"2022031216064760700_R48","doi-asserted-by":"crossref","unstructured":"Kahn SE, Leonetti DL, Prigeon RL, Bergstrom RW, Fujimoto WY: Proinsulin as a marker for the development of NIDDM in Japanese-American men. Diabetes\u200844:173\u2013179, 1995","DOI":"10.2337\/diabetes.44.2.173"},{"key":"2022031216064760700_R49","doi-asserted-by":"crossref","unstructured":"Mykkanen L, Haffner SM, Kuusisto J, Pyorala K, Hales CN, Laakso M: Serum proinsulin levels are disproportionately increased in elderly prediabetic subjects. Diabetologia\u200838:1176\u20131182, 1995","DOI":"10.1007\/BF00422366"}],"container-title":["Diabetes Care"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/diabetesjournals.org\/care\/article-pdf\/25\/2\/292\/649434\/dc0202000292.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https:\/\/diabetesjournals.org\/care\/article-pdf\/25\/2\/292\/649434\/dc0202000292.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2022,3,12]],"date-time":"2022-03-12T16:26:47Z","timestamp":1647102407000},"score":1,"resource":{"primary":{"URL":"https:\/\/diabetesjournals.org\/care\/article\/25\/2\/292\/23340\/Insulin-and-Amylin-Release-Are-Both-Diminished-in"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2002,2,1]]},"references-count":49,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2002,2,1]]}},"URL":"https:\/\/doi.org\/10.2337\/diacare.25.2.292","relation":{},"ISSN":["0149-5992","1935-5548"],"issn-type":[{"value":"0149-5992","type":"print"},{"value":"1935-5548","type":"electronic"}],"subject":[],"published":{"date-parts":[[2002,2,1]]}}}