Abstract
There is now considerable evidence that increased hepatic glucose output rather than reduced peripheral glucose uptake is the primary factor responsible for both fasting and postprandial hyperglycemia in type 2 diabetes1,2. It is, therefore, appropriate to consider the mechanisms that may be involved in permitting and promoting this excessive hepatic output of glucose.
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References
J.E. Gerich, Is muscle the major site of insulin resistance in type 2 (noninsulin-dependent) diabetes mellitus?, Diabetologia. 34:607–610 (1991).
A. Mitrakou, D. Kelley, T. Veneman, T. Jenssen, T. Pangburn, J. Reilly, and J. Gerich, Contribution of abnormal muscle and liver glucose metabolism to postprandial hyperglycemia in noninsulin-dependent diabetes mellitus, Diabetes. 39:1381–1390 (1990).
J. Wahren, P. Felig, E. Cerasi, and R. Luft, Splanchnic and peripheral glucose and amino acid metabolism in diabetes mellitus, J Clin Invest, 51:1870–1878 (1972).
R.H. Chochinov, H.F. Bowen, and J.A. Moorhouse, Circulating alanine disposal in diabetes mellitus, Diabetes. 27:420–426 (1978).
R.C. DeMeutter and W.W. Eeve, Conversion of DL-lactate-2-14C or pyruvate-2-14C to blood glucose in humans: effect of diabetes, insulin, tolbutamide and glucose load, J Clin Invest. 42:523–533 (1963).
G.A. Reichard, F.N. Moury, N.J. Hochella, A.L. Patterson and S. Weinhouse, Quantitative estimation of the Cori Cycle in humans, J Biochem. 238:495–501 (1963).
C. Waterhouse and J. Keilson, The contribution of glucose to alanine metabolism in man, J Lab Clin Med. 92:803–812 (1978).
J. Zawadski, R. Wolfe, D. Mott, S. Lillioja, B. Howard and C. Bogardus, Increased rate of Cori Cycle in obese subjects with NIDDM and effects of weight reduction, Diabetes. 37:154–159 (1988).
J. Katz, Determination of gluconeogenesis in vivo with [14C]-labelled substrates, Am J Physiol. 248:R331–R339 (1985).
A. Consoli, N. Nurjhan, F. Capani, and J.E. Gerich, Predominant role of gluconeogenesis in increased hepatic glucose production in NIDDM, Diabetes. 38(5) 550–557 (1989).
C. Desrosiers, F. David, M. Garneau and H. Brunengraber, Nonhomogeneous labeling of liver mitochondrial acetyle CoA, J Biol Chem. 266:1574–1578 (1991).
W. Schumann, I. Magnusson, V. Chandramouli, K. Kumaran, J. Wahren and B. Landau, Metabolism of [2-14C] acetate and its use in assessing hepatic Krebs cycle activity and gluconeogenesis, J Biol Chem. 266:6985–6990 (1991).
A. Consoli, N. Nurjhan, J. Reilly, D. Bier, and J. Gerich, Mechanism of increased gluconeogenesis in noninsulin-dependent diabetes mellitus, J Clin Invest. 86:2038–2045 (1990).
M. Korytkowski, A. Consoli, W. Pimenta, and J. Gerich, Pathogenesis of fasting hyperglycemia in NIDDM, Diabetes. 41(1): 10(A)#40 (1992) (Abstract).
N. Nurjhan, A. Consoli, and J. Gerich, Increased lipolysis and its consequences on gluconeogenesis in noninsulin-dependent diabetes mellitus, J Clin Invest. 89:169–175 (1992).
A. Virkamaki, I. Puhakainen, N. Nurjhan, J. Gerich and H. Yki-Jarvinen, Measurement of lactate formation from glucose using [6-3H] and [6-14C] glucose in humans, Am J Physiol. 259:397–404 (1990).
R. Kreisberg, Glucose-lactate interrelations in man, N Engl J Med. 287:132–137 (1972).
P. Felig, The glucose-alanine cycle, Metabolism. 22:179–207 (1973).
A. Bucci, I. Toft, T. Jenssen, D. Bier, and N. Nurjhan, Glutamine metabolism an its contribution to glucose and alanine production in man, Diabetes. 41(1):68A;#249 (1992) (Abstract).
N. Nurjhan, F. Kennedy, A. Consoli, C. Martin, J. Miles and J. Gerich, Quantification of the glycolytic origin in plasma glycerol as an index of lipolysis in vivo, Metabolism. 37:371–377 (1988).
J. Katz and J. McGarry, The glucose paradox: is glucose a substrate for liver metabolism, J Clin Invest. 74:1901–1909 (1984).
N. Nurjahan, Diabetologia. 33:A1–A4 (1990).
P. Campbell, G. Bolli, and J. Gerich, Quantification of the relative impairment in actions of insulin on hepatic glucose production and peripheral glucose uptake in noninsulin-dependent diabetes mellitus, Metabolism. 37:15–22 (1988).
A. Mitrakou, D. Kelley, T. Veneman, T. Pangburn, J. Reilly, and J. Gerich, Role of reduced suppression of hepatic glucose output and diminished early insulin release in impaired glucose tolerance, N Engl J Med. 326:22–29 (1992).
A.R. Baron, L. Schaeffer, P. Shragg and O.G. Kolterman, Role of hyperglucogenesis in maintenance of increased rates of hepatic glucose output in type 2 diabetes, Diabetes. 36:274–283 (1987).
R. Unger and L. Orci, Physiology and pathophysiology of glucagon, Physiol Rev. 56:779–826 (1976).
J. Williamson, R. Kreisberg, and P. Felta, Mechanism for the stimulation of gluconeogenesis by fatty acids in perfused rat liver, Proc Nat’l Acad Sci. 56:247–254 (1966).
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Gerich, J.E., Nurjhan, N. (1993). Gluconeogenesis in Type 2 Diabetes. In: Östenson, C.G., Efendić, S., Vranic, M. (eds) New Concepts in the Pathogenesis of NIDDM. Advances in Experimental Medicine and Biology, vol 334. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2910-1_18
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DOI: https://doi.org/10.1007/978-1-4615-2910-1_18
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