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Body Fat & Bone Loss: lipoatrophy & belly fat accumulation BOTH lead to bone loss
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.......this certainly helps to explain the high rates of bone loss in HIV at an early age, as in many studies osteopenia rates of 50% and osteoporosis rates of 5-15% in HIV+ individuals at the stunning average age of 45 yrs old have been observed. This also helps to understand why insulin resistance & diabetes are associated with increased risk for bone loss!!!
Lipodystrophy & Bone Loss
Whereas insulin resistance, type 2 diabetes, and arteriosclerosis have previously been linked to osteopenia, the detrimental relationship of VAF to bone ...
www.nat ap.org/2009/HIV/090609_03.htm
Lipoatrophy increases bone loss risk and visceral fat also increases bone loss: This study finds higher levels of subcutaneous fat are protective of bone loss, while more visceral fat (belly fat) increases bone loss......adipose tissue is the source of a number of hormones, cytokines, and inflammatory factors that modulate multiple biological functions and have depot-specific differences in gene expression
Low body weight and recent weight loss are well-known risk factors for osteoporosis and fractures......
A consistent body of literature suggests the pattern of regional fat deposition into the sc and visceral compartments to be a stronger predictor of disease risk than overall fat mass.....Secretions from visceral adiposity pass through the liver before entering general circulation, uniquely implicating intraabdominal fat in the pathogenesis of insulin resistance and type 2 diabetes.......
We found that visceral and sc fat have opposite effects on the appendicular skeleton; whereas sc fat is beneficial to bone structure and strength, visceral fat serves as an unique pathogenic fat depot.......We found, however, that even in healthy young women with weights between the 3rd and 97th percentiles, VAF (visceral adipose fat) is negatively correlated with the amount and strength of bone in the appendicular skeleton......adipose tissue is the source of a number of hormones, cytokines, and inflammatory factors that modulate multiple biological functions and have depot-specific differences in gene expression......Proteins that are potentially protective against the development of osteoporosis, such as adiponectin, have lower levels of expression in visceral than sc fat tissue.....Leptin, a satiety-regulating hormone that is produced by adipocytes, promotes the differentiation of osteoblasts, and affects bone resorption, is also supposedly less abundant in visceral tissue......the expression of aromatase, which converts androgen to estrogen and results in reduced osteoclast activity is known to be lower in visceral adipocytes (6). In contrast, visceral adiposity is associated with increased levels of proinflammatory cytokines, (37, 38, 39) like TNF-{alpha} and IL-6, both of which increase bone res orption and promote osteoporosis (40)."
Increased VAF (visceral fat) is associated with insulin resistance and dyslipidemia and is an independent risk factor for type 2 diabetes, myocardial infarction, hypertension, and all-cause mortality. Whereas insulin resistance, type 2 diabetes, and arteriosclerosis have previously been linked to osteopenia, the detrimental relationship of VAF to bone mass in nonobese, nondiabetic populations has not been carefully examined. We found, however, that even in healthy young women with weights between the 3rd and 97th percentiles, VAF is negatively correlated with the amount and strength of bone in the appendicular skeleton.
Our results, suggesting the influence of fat on bone to be foremost dependent on the site in which it accumulate s, may help explain the large body of conflicting data on the link between body adiposity and bone mass
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Fracture Risk Demands Attention in Diabetes Patients
By Crystal Phend, Senior Staff Writer, MedPage Today
Published: September 24, 2010
STOCKHOLM -- Because type 2 diabetes weakens the bone in often undetectable ways, both directly and indirectly via treatment side effects, experts here urged increased awareness.
Fracture has gained attention as a complication of the thiazolidinediones, but bone complications remain under-recognized in diabetes overall, P er-Henrik Groop, MD, DMSc, of the University of Helsinki, told reporters at a press conference at the European Association for the Study of Diabetes meeting.
One big part of the problem is the "invisible" damage, explained Peter Vestergaard, MD, PhD, of Aarhus University Hospital in Aarhus, Denmark.
"Before you are able to do something about a problem you need to be aware that it's there," he told reporters.
Typically, osteoporosis can be monitored through progressively declining bone mineral density. But Vestergaard's research has revealed greater structural frailty of bone in diabetes than expected for a given level of bone mineralization.
"When you measure in diabetics, their bone may look like normal bone at least under the scanners we use nowadays," he said at the press conference. "However, it fractures."
The biomechanical problems with bones in diabetes patients aren't fully understood yet, but the collagen that give bone its flexibility appears to be implicated, Vestergaard noted.
"But it seems like the glucose in a way 'caramelizes' the bone," he explained at the press conference.
Standard DEXA scanners currently can't pick up these issues, so Vestergaard and other researchers are considering bone biopsy and 3D scanners to figure out how to reinterpret standard diabetic scans.
Another route being explored to explain the interaction is a hormone called osteocalcin which appears to be a way in which bone affects diabetes, as Patricia F. Ducy, PhD, of Columbia University in New York City, discussed at the press conference.
This hormone is made exclusively in bone, then goes through the blood to the pancreas where it increases beta cell proliferation and insulin levels, thereby improving insulin sensitivity, she explained.
"Bone is not only a receiver but a giver," she told reporters.
Osteocalcin may be a new molecule that could be exploited in the treatment of diabetes, she suggested, noting animal model studies that show benefits of osteocalcin administration.
"It is a long way from the lab to the clinic but it is a pathway we should at least investigate," she said.
Of course, diabetes treatments can also influence bone complications -- namely fracture -- indirectly through hypoglycemia as especially elderly patients are at risk of falls when glucose levels get too low, added Matteo Monami, MD, PhD, of the University of Florence, Italy.
"We have to consider bone fractures among treatment outcome for choice of hyperglycemic treatment options," especially for postmenopausal women, who are already at elevated risk, he said at the press conference.
Vestergaard reported receiving travel grants fro m Eli Lilly, Servier, and Novartis; speakers' fees from sanofi-aventis; and research grants from Servier.
Monami reported receiving speakers' fees from GlaxoSmithKline, Takeda, Novo Nordisk, sanofi-aventis, Eli Lilly, Merck Sharp Dohme, Bristol-Myers Squibb, and Novartis.
Ducy reported being a consultant for Escoublac.
Groop reported having no relevant conflicts of interest to disclose.
Primary source: European Association for the Study of Diabetes
Source reference:
Groop PH, et al "Diabetes and the bone" EASD 2010.
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