Rethinking peer support for diabetes in Vancouver's South-Asian community: a feasibility study.

AIM: To examine the feasibility and potential health impact of a diabetes self-management education and support intervention involving peer support on glycaemic control and diabetes distress. METHODS: A total of 41 South-Asian adults with Type 2 diabetes were recruited for a 24-week diabetes self-management education and support pilot intervention involving peer support. The intervention consisted of six weekly education sessions co-facilitated by a certified diabetes educator and two peer leaders, followed by 18 weekly support sessions facilitated by two peer leaders. Education sessions were guided entirely by participants' self-management questions and also emphasized goal setting and action planning. Support sessions were based on empowerment principles and participants discussed self-management challenges, shared emotions, asked self-management questions, problem-solved in a group, set goals, and developed and evaluated action plans. Feasibility outcomes included recruitment and retention. Primary health-related outcomes included HbA1c levels and diabetes distress (measured at baseline, 6 and 24 weeks). Programme satisfaction was also assessed. RESULTS: Pre-established criteria for recruitment and retention were met. Paired t-tests showed no changes in HbA1c and diabetes distress at 6 weeks. At 24 weeks, HbA1c levels deteriorated [54 mmol/mol (7.1%) vs 61 mmol/mol (7.7%)] while diabetes distress scores improved (2.0 vs 1.7). CONCLUSIONS: Although feasible, findings suggest this peer-support model may have a positive impact on diabetes distress, but not on HbA1c levels. Culturally responsive modifications (e.g. intervention location) to the pilot model are needed and could lead to more favourable health outcomes for this community. Such a re-designed peer-support model will require further investigation.

Evaluating a diabetes self-management support peer leader training programme for the English- and Punjabi-speaking South-Asian community in Vancouver.

AIMS: The purpose of this single-cohort study was to implement and evaluate a programme that trains peers to deliver a diabetes self-management support programme for South-Asian adults with Type 2 diabetes and to assess the perceived efficacy of and satisfaction with this programme. METHODS: We recruited eight South-Asian adults who completed a 20-h peer-leader training programme conducted over five sessions (4 h per session). The programme used multiple instructional methods (quizzes, group brainstorming, skill building, group sharing, role-play and facilitation simulation) and provided communication, facilitation, and behaviour change skills training. To graduate, participants were required to achieve the pre-established competency criteria in four training domains: active listening, empowerment-based facilitation, five-step behavioural goal-setting, and self-efficacy. Participants were given three attempts to pass each competency domain. RESULTS: On the first attempt six (75%), eight (100%), five (63%) and five (63%) participants passed active listening, empowerment-based facilitation, five-step behavioural goal-setting, and self-efficacy, respectively. Those participants who did not pass a competency domain on the first attempt were successful in passing on the second attempt. As a result, all eight participants graduated from the training programme and became peer leaders. Satisfaction ratings for programme length, balance between content and skills development, and preparation for leading support activities were uniformly high. Ratings for the instructional methods ranged between effective and very effective. CONCLUSION: Findings suggest it is feasible to train and graduate peer leaders with the necessary skills to facilitate a diabetes self-management support intervention.

Dietary omega 3 fatty acid alters prostaglandin synthesis, glucose transport and protein turnover in skeletal muscle of healthy and diabetic rats.

The present study was designed to determine if dietary-fat-induced alterations in the fatty acid composition of skeletal-muscle lipid alters insulin-dependent and basal muscle metabolism, including glucose and amino acid transport, prostaglandin (PG) synthesis and protein turnover. Rats were fed on high-fat semi-purified diets providing 19% or 1% omega 3 fatty acids in the form of fish oil, for 6 weeks. After 3 weeks, half of the rats were made diabetic by a single injection of streptozotocin (50 mg/kg body wt.). After a further 3 weeks, contralateral epitrochlearis and extensor digitorum longus (EDL) muscles from each rat were incubated in vitro. High levels of dietary omega 3 fatty acids decreased PGE2 and PGF2 alpha synthesis in EDL and epitrochlearis muscle (P less than 0.0001). Diabetes and insulin had no effect on PG synthesis. Diet did not alter basal glucose or amino acid transport in EDL muscle from healthy or diabetic rats. Insulin increased glucose and amino acid transport (P less than 0.0001); the increase in glucose transport by insulin was significantly greater in muscles of rats fed on high levels of omega 3 fatty acids (P less than 0.05). Epitrochlearis from rats fed on high levels of omega 3 fatty acids showed decreased net protein degradation in the presence and absence of insulin, owing to decreased rates of protein degradation and synthesis. The data suggest that high levels of dietary omega 3 fatty acids that alter muscle membrane composition also result in alterations in glucose transport and the metabolism of muscle protein.

Comparison of the lipid regulation of yeast and rat CTP: phosphocholine cytidylyltransferase expressed in COS cells.

The CTP: phosphocholine cytidylyltransferase (CT) gene from yeast and cDNA from rat liver were over-expressed 20-30-fold in COS cells. Most of the CT activities were found in the cytosolic fraction. The regulation of the yeast CT activity (Y-CT) by lipids was characterized for the first time in comparison with the regulation of the well-studied rat CT (R-CT). Sonicated vesicles composed of egg phosphatidylcholine (PC) or 1-stearoyl-2-oleoyl PC had no effect on Y-CT and only slightly stimulated R-CT activity. Both CTs were activated 10-50-fold by the anionic lipids cardiolipin, phosphatidyl-glycerol, phosphatidylinositol and oleic acid. The effects of varying the vesicle concentration and the mol% of anionic lipid in PC vesicles were tested. The concentration optima for the activation of Y-CT by oleic acid or anionic phospholipids were 5-10-fold lower than those for R-CT. For example, the stimulation of Y-CT activity by phosphatidylglycerol vesicles was optimal between 5 and 15 microM and declined at higher concentrations, but R-CT activation by these vesicles saturated at approximately 25 microM. The positively charged aminolipid sphingosine antagonized the stimulation by oleic acid of both Y-CT and R-CT. Y-CT activity was insensitive to PC vesicles containing the neutral lipids diacylglycerol, monoacylglycerol or oleyl alcohol. However, R-CT was stimulated 10-20-fold by vesicles containing these neutral lipids. Translocation of the CTs to microsomal membranes enriched with anionic or neutral lipids was compared. Oleic acid enrichment promoted translocation of Y-CT and R-CT, whereas diacylglycerol promoted only R-CT translocation. These data show that the activity of Y-CT is lipid-sensitive. Y-CT is affected only by charged lipids, whereas R-CT responds to charged and neutral lipid activators. The data are consistent with different modes of interaction of the two CTs with lipids.

Sphingosine inhibits the activity of rat liver CTP:phosphocholine cytidylyltransferase.

We report CTP:phosphocholine cytidylyltransferase (CT) as another target enzyme of sphingosine actions in addition to the well-characterized protein kinase C. Effects of sphingosine and lysophingolipids were studied on the activity of purified cytidylyltransferase prepared by the method of Weinhold et al. (Weinhold, P. A., Rounsifer, M.E., and Feldman, D.A. (1986) J. Biol. Chem. 261, 5104-5110). The sphingolipids were tested as components of egg phosphatidylcholine (PC) vesicles, 25 mol% sphingosine inhibited the CT activity by about 50%. The inhibition of CT by sphingosine and lysosphingolipids was reversible. Sphingosine was found to be a reversible inhibitor of CT with respect to the activating lipids such as phosphatidylserine, phosphatidylinositol, phosphatidylglycerol, and fatty acid:phosphatidylcholine vesicles. Egg PC vesicles containing sphingosine, psychosine (galactosylsphingosine), glucopsychosine (glucosylsphingosine), and lysosphingomyelin (sphingosylphosphorylcholine) suppressed the activation by PC/oleic acid vesicles, whereas the parent sphingolipids did not. Egg PC vesicles containing oleylamine and hexadecyltrimethylamine inhibited CT activity, whereas egg PC-octylamine vesicles did not alter the enzyme activity. This indicates the importance of an amino group and long alkyl chain. LysoPC, a known detergent, did not inhibit the enzyme activity under the same assay conditions in which sphingosine inhibited. These results are the first report of a lipid inhibitor of purified CT.

Effects of diet and selected hormones on the activities of hepatic malic enzyme and glucose-6-phosphate dehydrogenase in infant, prematurely weaned rats.

Male Sprague-Dawley rats were weaned on postnatal d 17 to isocaloric diets in which fat supplied either 10% (PWC group) or 65% (PWF group) of the available energy. Compared with animals left with the dams to be weaned spontaneously to the maternal low fat diet (SWC group), the PWC rats showed early increases in the activities of liver glucose-6-phosphate dehydrogenase (G-6-PD) and malic enzyme (ME). The activity of G-6-PD was diminished in the PWF group, but the early rise in liver ME activity attendant on premature weaning was not prevented. Premature weaning, regardless of diet, decreased plasma glucagon levels within 1 d. Hydrocortisone failed to evoke hepatic ME activity in SWC rats; similarly, corticosterone and insulin, separately or together, did not affect ME activity in SWC rats. However, triiodothyronine evoked hepatic ME appearance within 1 d. Glucagon suppressed the expected rise in hepatic ME activity in PWC rats; in contrast, injection of glucagon antiserum into SWC rats led to the appearance of liver ME within 2 d. The data indicated that interaction among diet, glucagon and thyroid hormones may be part of the mechanism regulating the first appearance of ME in rat liver.