Post-fracture care programs for prevention of subsequent fragility fractures: a literature assessment of current trends.

Post-fracture care (PFC) programs evaluate and manage patients with a minimal trauma or fragility fracture to prevent subsequent fractures. We conducted a literature review to understand current trends in PFC publications, evaluate key characteristics of PFC programs, and assess their clinical effectiveness, geographic variations, and cost-effectiveness. We performed a search for peer-reviewed articles published between January 2003 and December 2020 listed in PubMed or Google Scholar. We categorized identified articles into 4 non-mutually exclusive PFC subtopics based on keywords and abstract content: PFC Types, PFC Effectiveness/Success, PFC Geography, and PFC Economics. The literature search identified 784 eligible articles. Most articles fit into multiple PFC subtopics (PFC Types, 597; PFC Effectiveness/Success, 579; PFC Geography, 255; and PFC Economics, 98). The number of publications describing how PFC programs can improve osteoporosis treatment rates has markedly increased since 2003; however, publication gaps remain, including low numbers of publications from some countries with reported high rates of osteoporosis and/or hip fractures. Fracture liaison services and geriatric/orthogeriatric services were the most common models of PFC programs, and both were shown to be cost-effective. We identified a need to expand and refine PFC programs and to standardize patient identification and reporting on quality improvement measures. Although there is an increasing awareness of the importance of PFC programs, publication gaps remain in most countries. Improvements in established PFC programs and implementation of new PFC programs are still needed to enhance equitable patient care to prevent occurrence of subsequent fractures.

Regulation of hepatic insulin receptors by pancreatic polypeptide in fasting and feeding.

Pancreatic polypeptide (PP) increases hepatic insulin receptor (IR) binding activity in fasted PP-deficient rats, but not fasted normal animals. PP-induced alteration of hepatic IR levels in normal animals may be detectable in the fed state when IR concentrations are lower than during fasting. In the current study, the effect of exogenous PP on IR concentrations in the fed and fasted states was determined in healthy 300- to 350-g male Sprague-Dawley rats. Ten animals were administered PP 100 microgram/kg/day for 3 days by intraperitoneal injection and 10 weight-matched control animals received saline vehicle. Five PP- and five saline-administered rats were fasted for 12 hr prior to organ procurement, while 5 PP- and 5 saline-treated rats were given free access to food for this period. Livers were removed and snap-frozen. IRs were isolated from solubilized hepatocyte membranes by affinity chromatography with agarose-bound wheat germ agglutinin. Western blots were performed using a specific antibody to the beta subunit of the IR, which was detected by a chemiluminescence technique after 45-min exposure to X-ray film. Exposed films were examined by scanning densitometry and IR concentration was expressed as absorbance units per milligram of hepatic protein (mean +/- SE). Statistical comparisons were by Student's t test with significance taken at P < 0.05. Feeding was associated with a significantly lower IR concentration in saline-administered animals compared with the fasted state (24.2 +/- 4.0 vs 53.3 +/- 11.1). PP administration in fed rats resulted in significantly increased IR concentration as compared with that seen in saline-administered fed animals (43.8 +/- 8.9 vs 24.2 +/- 4.0). This difference may be due to increased IR synthesis with long-term PP administration, and supports the role of PP as a regulatory factor in hepatic carbohydrate metabolism.

Alterations in hepatocyte insulin binding in chronic pancreatitis: effects of pancreatic polypeptide.

BACKGROUND: Hepatic insulin resistance has previously been demonstrated in chronic pancreatitis, and has been shown to be ameliorated by pancreatic polypeptide administration. Insulin binding was investigated in chronic pancreatitis induced by infusion of oleic acid into the pancreatic duct of rats. METHODS: Acute pancreatitis was induced in 12 200 to 225 g 8-week-old male Sprague-Dawley rats by intubation of the main bile duct at its junction with the duodenum through a small midline abdominal incision, and infusion of 99% oleic acid 0.015 mL/min for 4 minutes, with an additional 4 minutes dwell-time after infusion. Sham-operated animals served as controls. After 6 weeks, chronic pancreatitic and sham-operated animals received either intraperitoneal bovine pancreatic polypeptide or saline vehicle for 5 days. Intraduodenal glucose tolerance tests (GTT) were performed in fasted animals, after which tissues were procured. Insulin receptors were isolated from solubilized hepatocyte and rectus abdominus membranes and competitive-binding studies were performed by incubation with 125I-insulin. Dissociation coefficients (Kd) and maximum binding capacities (Bmax) for high-affinity receptors were derived from Scatchard analyses. RESULTS: Bmax and Kd in muscle were not altered in animals with chronic pancreatitis. In liver, Bmax was significantly less in rats with chronic pancreatitis given saline than in sham-operated rats given saline (17.0 +/- 6.3 versus 47.6 +/- 13.1 fmol/mg protein; data are mean +/- SEM). Pancreatic polypeptide administration increased hepatic Bmax in rats with chronic pancreatitis (to 47.2 +/- 9.8 fmol/mg protein), but had no significant effect in sham-operated rats. Receptor affinity was not significantly different in rats with chronic pancreatitis or rats who underwent sham operations and was unaltered by the administration of pancreatic polypeptide. The integrated plasma glucose response during the GTT was reduced by pancreatic polypeptide administration in rats with chronic pancreatitis (29.5 +/- 15.0 mg/dL per minute versus 69.0 +/- 21.8 in chronic pancreatitis without pancreatic polypeptide), but was not significantly altered in sham-operated animals. CONCLUSION: Diminished expression of high-affinity receptors on the hepatocyte membrane may contribute to hepatic insulin resistance in chronic pancreatitis. In this model, pancreatic polypeptide improved glucose tolerance and increased receptor capacity to the level observed in livers from nonpancreatitic animals.