Insulin-stimulated glucose utilization was estimated in vivo in 1.5-, 4-, and 12-mo-old rats with an insulin suppression test wherein the height of the steady-state plasma glucose ( SSPG ) concentration, at similar steady-state plasma insulin levels, provides a direct reflection of the efficiency of insulin-stimulated glucose disposal. In parallel studies, the effect of age on in vitro insulin-stimulated glucose uptake was assessed in perfused hindlimb preparations. In addition, changes in the activity of enzymes that regulate muscle glycolysis, glycogenesis, and glycogenolysis were determined in isolated soleus muscle. The results indicated that rats got heavier as they became older, and changes in weight were associated with parallel increases in mean (+/- SE) SSPG concentrations as rats grew from 1.5 (56 +/- 3 mg/dl) to 4 (172 +/- 6 mg/dl) to 12 mo of age (194 +/- 8 mg/dl). The age-related decline in in vivo insulin action was associated with a reduction in insulin action on muscle, and maximal insulin-stimulated glucose uptake by perfused hindlimbs of 12-mo-old rats was approximately 50% of the value seen with perfused hindlimbs from 1.5-mo-old rats. Soleus muscle enzyme activity also varied with age, with significant increases in glycogen synthase and decreases in glycogen phosphorylase documented. Furthermore, muscle glycogen phosphorylase activity, which fell during an insulin infusion in 1.5-mo-old rats, did not change when 12-mo-old rats were infused at comparable insulin levels. Finally, glycogen content was significantly increased (P less than 0.01) in soleus muscle from 12-mo-old rats.(ABSTRACT TRUNCATED AT 250 WORDS)

It has been reported that insulin secretion decreases during hypoxia both in vitro and in vitro, while an increase in glucagon secretion is found only in vivo. The effect of acute hypoxia on the secretion of glucagon and insulin was studied in the perfused rat pancreas. Phentolamine, an alpha-adrenergic blocker, was perfused during the period of hypoxia to elucidate the role of alpha-adrenergic stimulation. Sodium ATP and dibutyryl cAMP were also administered to study their effects on insulin and glucagon responses during hypoxia. In the present experiments, insulin secretion was suppressed while glucagon secretion was increased during hypoxia. Phentolamine did not cause any change in insulin of glucagon secretion. When dibutyryl cAMP was added, the increased glucagon secretion was reduced to the basal level, whereas the decreases in insulin secretion were not altered. The addition of sodium ATP reversed the hypoxia-induced decrease in insulin and the increase in glucagon secretion. These results suggest that a decrease in ATP production, which leads to impaired cAMP generation, pays a role in, and that alpha-adrenergic stimulation does not participate in the changes in, insulin and glucagon secretion during hypoxia in vitro.

A 51-year-old type 2 diabetic patient with a scrotal subcutaneous abscess is reported. He was diagnosed as having diabetes mellitus five years earlier. Hehad left scrotal swelling and pain with granulocytosis, elevated C-reactive protein and hyperglycemia. He was successfully treated with incision and drainage {Streptococcus agalactiae was identified in the pus), debridement, antibiotics, immunoglobulin and insulin. This case resembled Founder's gangrene, an infective necrotizing fasciitis of the perineal, genital or perianal regions. Diabetes mellitus is a basic disorder often associated with Founder's gangrene. Scrotal subcutaneous abscess should be prevented from progressing to Founder's gangrene with early and appropriate treatment. (Internal Medicine 39: 991-993, 2000)

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Plasma glucagon (IRG) response to different glucose levels in alloxan diabetic rats was studied. Glucose was given to normal and diabetic rats orally and then by infusion, and the amount of IRG secreted was measured. The experiment was also done on isolated rat pancreas which was perfused with glucose. Oral glucose load (0.3 g/100 g) produced a paradoxical rise in IRG in alloxan diabetic rats while no significant change was observed in normal rats. When glucose was infused (0.15 g/100 g as a bolus + 0.006 g/100 g/min) IRG secretion was inhibited over the entire period of the test in both normal and diabetic rats, but the inhibition observed in diabetic rats was weaker. However, in the isolated rat pancreas perfusion experiment, alloxan diabetic rat pancreas responded normally to increasing glucose concentration resulting in a decrease of IRG in the perfusate. When insulin was infused in vivo into diabetic rats that were given glucose orally, the paradoxical rise in IRG was prevented. In the case of rats that were given glucose by infusion, the addition of insulin lowered IRG levels. On the other hand, when glucose level was decreased to the state of hypoglycemia, a significant increase in IRG was observed in both normal and diabetic rats. From these results it is concluded that 1) paradoxical rise of IRG during oral glucose load is related to IRG secreted from gut in addition to that secreted from pancreas, 2) excess glucagon secretion from pancreas in alloxan diabetic rats can be inhibited by administrating large amount of insulin, however, 3) in the in vitro perfusion system, glucagon secretion was not influenced by insulin deficiency.