Introduction: Lipohypertrophies (LHs) due to incorrect insulin injection techniques have been described in the literature for decades. Their rate averages 38%, but this is still controversial because of the vast range reported by different publications, most of which fail to describe the selected detection protocol and therefore are not entirely reliable. We still need to identify the real LH rate, and only consistently using a standardized method in a large cohort of insulin-treated (IT) patients make this possible.

In this study, the authors demonstrate that rats with n-3 fatty acid deficiency display spatial learning deficits in the Barnes circular maze. Dams were deprived of n-3 fatty acids during pregnancy and lactation, and their offspring were weaned to the same deficient diet. There was a 58% loss of brain docosahexaenoic acid (DHA) in the n-3 fatty acid-deficient rats in comparison to n-3 fatty acid-adequate rats. At 8 weeks of age, deficient rats demonstrated moderate impairment in Barnes maze performance compared with the n-3 fatty acid-adequate rats during the initial training. In the reversal learning task, the n-3 fatty acid-deficient rats showed a profound deficit in performance: They required more time to find a new position of the escape tunnel, which was accompanied by a higher number of errors and perseverations. The n-3 fatty acid-deficient rats had reduced tissue levels of dopamine in the ventral striatum and enhanced levels of the metabolite 3,4-dihydroxyphenylacetic acid in frontal cortex and hypothalamus. In summary, this study demonstrates that rats with low brain DHA have a deficit in spatial reversal learning that could be related to changes in dopamine transmission in critical brain circuits.

Our previous work demonstrated that a decrease in brain docosahexaenoic acid (DHA) in rodents was associated with poorer performance in the Morris water maze. In this study we showed a deficit in spatial task performance of n‐3 deficient rats using the Barnes circular maze, which is similar to the Morris maze in that both tests require an escape response. Deficiency has been accomplished through the use of a two generational model in which the dam is deprived of n‐3 fatty acid sources and her offspring are then weaned to the same deficient diet. There was a loss of 56% of total brain DHA in n‐3 deficient (n‐3 Def) in comparison to n‐3 adequate (n‐3 Adq) rats. Both n‐3 Def (n=11) and n‐3 Adq (n=10) rats learned to locate the escape tunnel during the four days of training (2 trials a day), as indicated by a progressive reduction in escape latencies and errors rate. However, during the first two days, n‐3 Def rats did not perform as well as n‐3 Adq, but differences between groups did not reach the significance. To evaluate memory retention, rats were retested in the Barnes maze ten days after the last training trial. In the retention testing, n‐3 Adq rats did not differ from n‐3 Def in escape latencies (27.3+6.0 sec vs 24.9+7.2 sec)) and errors rate (4.55+1.2 vs 3.80+1.1). One week after memory retention testing, the escape tunnel was moved to a new position (opposite to the original), and rats were retrained in five consecutive trials to find the new location of the target (reversal learning). Def rats required more time to find the new position of the escape tunnel (p=0.003). This increase in the escape latencies was accompanied by a significantly higher number of errors. So, this study demonstrated a deficit in spatial task performance rats with low brain DHA in the two generational model. This project was funded by the Intramural Research Program of the NIAAA/NIH.

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