1128
complete linkage disequilibrium with myotonic dystrophy,6 such that all individuals with myotonic dystrophy have the same allele. This finding suggests that the original event (probably an increase from an allele with n 5-27 to one with n :., 50) may have resulted in minimal or no clinical disturbance, but that an adverse clinical outcome arose from enlargement of this allele in subsequent generations because of its instability. How this change produces the observed =
clinical effects on muscle and other symptoms is still to be determined, but the fmding of hereditary unstable DNA in patients with myotonic dystrophy helps to explain anticipation and variable manifestations among patients with this condition.
We thank Mr Lodewijk Sandkinjl and Dr lain Fenton for help with data and Dr Gertrude Kohn, Dr Dian Donnai, and Prof Victor Dubowitz for referring families. Our work is supported by the Muscular Dystrophy Group of Great Britain, Muscular Dystrophy Association and Piton Foundation (USA), the Wellcome Trust, and the Medical Research Council.
analysis,
REFERENCES 1.
Harper PS. Myotonic dystrophy. Philadelphia: Saunders, 1989.
Insulin resistance and
Cigarette smoking is associated with increases in plasma triglycerides and decreases in plasma high density-lipoprotein-cholesterol concentration. These changes not only increase risk of coronary heart disease but also are secondary to resistance to insulin-stimulated glucose uptake or hyperinsulinaemia. To see whether there is a relation between cigarette smoking and insulin-mediated glucose uptake we measured plasma lipid and
lipoprotein concentrations, plasma glucose and insulin response to an oral glucose challenge, and insulin-mediated glucose uptake in 40 matched healthy volunteers (20 non-smokers, 20 smokers). Smokers had significantly higher mean (SEM) very-low-density-lipoprotein triglycerides (0·66 [0·10] vs 0·39 [0·03] mmol/l, p
complete linkage disequilibrium with myotonic dystrophy,6 such that all individuals with myotonic dystrophy have the same allele. This finding suggests that the original event (probably an increase from an allele with n 5-27 to one with n :., 50) may have resulted in minimal or no clinical disturbance, but that an adverse clinical outcome arose from enlargement of this allele in subsequent generations because of its instability. How this change produces the observed =
clinical effects on muscle and other symptoms is still to be determined, but the fmding of hereditary unstable DNA in patients with myotonic dystrophy helps to explain anticipation and variable manifestations among patients with this condition.
We thank Mr Lodewijk Sandkinjl and Dr lain Fenton for help with data and Dr Gertrude Kohn, Dr Dian Donnai, and Prof Victor Dubowitz for referring families. Our work is supported by the Muscular Dystrophy Group of Great Britain, Muscular Dystrophy Association and Piton Foundation (USA), the Wellcome Trust, and the Medical Research Council.
analysis,
REFERENCES 1.
Harper PS. Myotonic dystrophy. Philadelphia: Saunders, 1989.
Insulin resistance and
Cigarette smoking is associated with increases in plasma triglycerides and decreases in plasma high density-lipoprotein-cholesterol concentration. These changes not only increase risk of coronary heart disease but also are secondary to resistance to insulin-stimulated glucose uptake or hyperinsulinaemia. To see whether there is a relation between cigarette smoking and insulin-mediated glucose uptake we measured plasma lipid and
lipoprotein concentrations, plasma glucose and insulin response to an oral glucose challenge, and insulin-mediated glucose uptake in 40 matched healthy volunteers (20 non-smokers, 20 smokers). Smokers had significantly higher mean (SEM) very-low-density-lipoprotein triglycerides (0·66 [0·10] vs 0·39 [0·03] mmol/l, p
